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1. Nielsen SK, Møllgård K, Clement CA, Veland IR, Awan A, Yoder BK, Novak I, Christensen ST: Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines. Dev Dyn; 2008 Aug;237(8):2039-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines.
  • Hedgehog (Hh) signaling controls pancreatic development and homeostasis; aberrant Hh signaling is associated with several pancreatic diseases.
  • Here we investigated the link between Hh signaling and primary cilia in the human developing pancreatic ducts and in cultures of human pancreatic duct adenocarcinoma cell lines, PANC-1 and CFPAC-1.
  • We show that the onset of Hh signaling from human embryogenesis to fetal development is associated with accumulation of Hh signaling components Smo and Gli2 in duct primary cilia and a reduction of Gli3 in the duct epithelium.
  • These findings indicate that primary cilia are involved in pancreatic development and postnatal tissue homeostasis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Cilia / metabolism. Hedgehog Proteins / metabolism. Pancreas / cytology. Pancreas / embryology. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Epithelial Cells / metabolism. Epithelial Cells / ultrastructure. Female. Fetus / cytology. Green Fluorescent Proteins / genetics. Humans. Kruppel-Like Transcription Factors / genetics. Kruppel-Like Transcription Factors / metabolism. Mice. NIH 3T3 Cells. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Pregnancy. Receptors, Cell Surface / metabolism. Receptors, G-Protein-Coupled. Transfection

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  • [Copyright] Copyright (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18629868.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 R01-HD056030
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI2 protein, human; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Nuclear Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / SHH protein, human; 0 / SMO protein, human; 0 / patched receptors; 147336-22-9 / Green Fluorescent Proteins
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2. Kelly KA, Bardeesy N, Anbazhagan R, Gurumurthy S, Berger J, Alencar H, Depinho RA, Mahmood U, Weissleder R: Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma. PLoS Med; 2008 Apr 15;5(4):e85
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  • [Title] Targeted nanoparticles for imaging incipient pancreatic ductal adenocarcinoma.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, typically presenting with metastasis at the time of diagnosis and exhibiting profound resistance to existing therapies.
  • METHODS AND FINDINGS: Here, a phage display approach was used in a mouse model of PDAC to screen for peptides that specifically bind to cell surface antigens on PDAC cells.
  • These screens yielded a motif that distinguishes PDAC cells from normal pancreatic duct cells in vitro, which, upon proteomics analysis, identified plectin-1 as a novel biomarker of PDAC.

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  • (PMID = 18416599.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA086355; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / K01 CA104647-03; United States / NCI NIH HHS / CA / P50-CA86355; United States / NCI NIH HHS / CA / P01-CA117969-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides; 0 / Plec protein, mouse; 0 / Plectin
  • [Other-IDs] NLM/ PMC2292750
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3. Fukushima N, Koopmann J, Sato N, Prasad N, Carvalho R, Leach SD, Hruban RH, Goggins M: Gene expression alterations in the non-neoplastic parenchyma adjacent to infiltrating pancreatic ductal adenocarcinoma. Mod Pathol; 2005 Jun;18(6):779-87
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  • [Title] Gene expression alterations in the non-neoplastic parenchyma adjacent to infiltrating pancreatic ductal adenocarcinoma.
  • The non-neoplastic pancreatic parenchyma adjacent to infiltrating ductal adenocarcinoma demonstrates inflammation, fibrosis, acinar cell loss and small duct-like metaplasia of acinar cells.
  • To better understand the pancreatic acinar responses to infiltrating pancreatic ductal adenocarcinoma, we characterized gene expression patterns of pancreatic acinar tissue adjacent to infiltrating pancreatic ductal adenocarcinomas and compared them to gene expression patterns of acinar tissue affected by chronic pancreatitis as well as to those of normal pancreatic acini.
  • Fresh-frozen pancreatic acinar tissue was microdissected from nine patients (three with pancreatic cancer, three with chronic pancreatitis, three with normal pancreata) using laser capture microdissection, and extracted RNA from each microdissection was subjected to two rounds of linear amplification and hybridized to oligonucleotide microarrays.
  • These 20 genes included pancreatitis-associated protein (HIP/PAP), a gene known to be overexpressed in acini adjacent to infiltrating pancreatic cancer, and the gene cartilage glycoprotein-39 (HC gp-39 or TKL-40).
  • Serum HC gp-39 protein levels were significantly higher in patients with pancreatic cancer and in those with chronic pancreatitis than in controls without pancreatic disease.
  • There was no significant difference in the levels of serum HC gp-39 in patients with pancreatic cancer and those with chronic pancreatitis.
  • Our results demonstrate some of the molecular alterations in acinar cells that occur in response to adjacent infiltrating pancreatic ductal adenocarcinoma and reveal that such alterations can provide a rich source of markers of pancreatic cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Gene Expression Profiling. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 15791284.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / CHI3L1 protein, human; 0 / Glycoproteins; 0 / Lectins; 0 / RNA, Neoplasm
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4. Michienzi S, Bucci B, Verga Falzacappa C, Patriarca V, Stigliano A, Panacchia L, Brunetti E, Toscano V, Misiti S: 3,3',5-Triiodo-L-thyronine inhibits ductal pancreatic adenocarcinoma proliferation improving the cytotoxic effect of chemotherapy. J Endocrinol; 2007 May;193(2):209-23
Hazardous Substances Data Bank. LIOTHYRONINE .

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  • [Title] 3,3',5-Triiodo-L-thyronine inhibits ductal pancreatic adenocarcinoma proliferation improving the cytotoxic effect of chemotherapy.
  • The pancreatic adenocarcinoma is an aggressive and devastating disease, which is characterized by invasiveness, rapid progression, and profound resistance to actual treatments, including chemotherapy and radiotherapy.
  • Several studies have shown that thyroid hormone, 3,3',5-triiodo-l-thyronine (T(3)) is able to promote or inhibit cell proliferation in a cell type-dependent manner.
  • The aim of the present study is to investigate the ability of T(3) to reduce the cell growth of the human pancreatic duct cell lines chosen, and to increase the effect of chemotherapeutic drugs at conventional concentrations.
  • Three human cell lines hPANC-1, Capan1, and HPAC have been used as experimental models to investigate the T(3) effects on pancreatic adenocarcinoma cell proliferation.
  • The hPANC-1 and Capan1 cell proliferation was significantly reduced, while the hormone treatment was ineffective for HPAC cells.
  • The T(3)-dependent cell growth inhibition was also confirmed by fluorescent activated cell sorting analysis and by cell cycle-related molecule analysis.
  • A synergic effect of T(3) and chemotherapy was demonstrated by cell kinetic experiments performed at different times and by the traditional isobologram method.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Pancreatic Neoplasms / drug therapy. Triiodothyronine / therapeutic use
  • [MeSH-minor] Antimetabolites / therapeutic use. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cisplatin / therapeutic use. Cyclin D1 / analysis. Cyclin D2. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Cyclins / analysis. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Drug Synergism. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. Fluorouracil / therapeutic use. Humans. Protein-Serine-Threonine Kinases / analysis. Receptors, Thyroid Hormone / analysis. p21-Activated Kinases

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  • (PMID = 17470512.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Thyroid Hormone; 06LU7C9H1V / Triiodothyronine; 0W860991D6 / Deoxycytidine; 136601-57-5 / Cyclin D1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; B76N6SBZ8R / gemcitabine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / p21-Activated Kinases; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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5. Karafin MS, Cummings CT, Fu B, Iacobuzio-Donahue CA: The developmental transcription factor Gata4 is overexpressed in pancreatic ductal adenocarcinoma. Int J Clin Exp Pathol; 2009 Aug 30;3(1):47-55
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  • [Title] The developmental transcription factor Gata4 is overexpressed in pancreatic ductal adenocarcinoma.
  • GATA4 is a transcription factor that plays a role in regulating the normal development of many mesoderm and endoderm derived tissues, including the pancreas.
  • By contrast, GATA4 mRNA expression is upregulated in pancreatic cancer cell lines and tissues.
  • To further clarify the relationship of GATA4 to pancreatic cancer, we immunolabeled 90 samples of pancreatic ductal adenocarcinoma using a GATA4 specific monoclonal antibody.
  • Samples of normal adult (n=26) and fetal pancreatic tissue (n=8) were also immunolabeled for comparison to expression patterns in pancreatic carcinoma tissues.
  • Immunolabeling for GATA4 indicated robust nuclear expression in developing acini in fetal pancreatic tissues, consistent with the role of GATA4 in embryologic development, and in mature pancreatic acinar epithelium.
  • Immunolabeling for GATA4 was also noted within normal duct epithelial cells, although it was always lesser in intensity than for acinar cell nuclei in the same section.
  • Positive GATA4 immunolabeling was seen in 61/90 (68%) infiltrating pancreatic cancers of which 27/90 (30%) showed strong positive labeling.
  • These findings support previous studies implicating GATA4 in pancreatic cancer and offer new avenues for investigation into this aggressive tumor type.

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  • (PMID = 19918328.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA106610; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA106610; United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2776266
  • [Keywords] NOTNLM ; Pancreatic cancer / development / embryology / transcription factor
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6. Radulovich N, Pham NA, Strumpf D, Leung L, Xie W, Jurisica I, Tsao MS: Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma. Mol Cancer; 2010 Feb 01;9:24
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  • [Title] Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma.
  • BACKGROUND: The cyclin D1 (CCND1) and cyclin D3 (CCND3) are frequently co-overexpressed in pancreatic ductal adenocarcinoma (PDAC).
  • RESULTS: CCND1 and CCND3 expression were selectively suppressed by shRNA in PDAC cell lines with expression levels of equal CCND1 and CCND3 (BxPC3), enhanced CCND1 (HPAC) or enhanced CCND3 (PANC1).
  • Suppression of cell proliferation was greater with CCND3 than CCND1 downregulation.
  • The downregulated gene targets in CCND3 suppressed cells were significantly enriched in cell cycle associated processes (p < 0.005).
  • CONCLUSIONS: Our results suggest that CCND3 is the primary driver of the cell cycle, in cooperation with CCND1 that integrates extracellular mitogenic signaling.
  • We also present evidence that CCND1 plays a role in tumor cell migration.
  • The results provide novel insights for common and differential targets of CCND1 and CCND3 overexpression during pancreatic duct cell carcinogenesis.

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  • (PMID = 20113529.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-49585
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / CCND1 protein, human; 0 / CCND3 protein, human; 0 / Cyclin D3; 136601-57-5 / Cyclin D1; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2824633
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7. Pham NA, Schwock J, Iakovlev V, Pond G, Hedley DW, Tsao MS: Immunohistochemical analysis of changes in signaling pathway activation downstream of growth factor receptors in pancreatic duct cell carcinogenesis. BMC Cancer; 2008;8:43
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  • [Title] Immunohistochemical analysis of changes in signaling pathway activation downstream of growth factor receptors in pancreatic duct cell carcinogenesis.
  • BACKGROUND: The pathogenesis of pancreatic ductal adenocarcinoma (PDAC) involves multi-stage development of molecular aberrations affecting signaling pathways that regulate cancer growth and progression.
  • This study was performed to gain a better understanding of the abnormal signaling that occurs in PDAC compared with normal duct epithelia.
  • METHODS: We performed immunohistochemistry on a tissue microarray of 26 PDAC, 13 normal appearing adjacent pancreatic ductal epithelia, and 12 normal non-PDAC ducts.
  • High levels of PKBbeta/AKT2, EGFR, as well as nuclear T202/Y204p-ERK and T180/Y182p-p38 were observed in normal ducts adjacent to PDAC compared with non-cancerous pancreas.
  • CONCLUSION: Multiple signaling proteins are activated in pancreatic duct cell carcinogenesis including those associated with the ERK, PKB/AKT, mTOR and STAT3 pathways.
  • The ERK pathway activation appears also increased in duct epithelia adjacent to carcinoma, suggesting tumor micro-environmental effects.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Blood Proteins / metabolism. Cell Nucleus / metabolism. Cytoplasm / metabolism. Disease Progression. Epithelium / metabolism. Humans. Immunohistochemistry. Pancreas / metabolism. Reference Values


8. Fu XM, Dai X, Ding J, Zhu BT: Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions. J Mol Histol; 2009 Jun;40(3):189-99
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  • [Title] Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions.
  • However, the pancreas-specific PDI homolog was previously suggested to be exclusively expressed in the pancreas (thus commonly referred to as PDIp).
  • Notably, in the digestive organs, such as the stomach and pancreas, very high levels of PDIp were selectively expressed in the digestive enzyme-secreting cells (e.g., gastric chief cells and pancreatic acinar cells).
  • In addition, high levels of PDIp expression were also detected in normal human pancreas, but its expression was mostly absent in human pancreatic duct adenocarcinoma and pancreatic cancer cell lines.
  • The absence of PDIp expression in pancreatic adenocarcinoma may serve as an additional biomarker for pancreatic cancer.

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  • (PMID = 19821078.001).
  • [ISSN] 1567-2387
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097109; United States / NCI NIH HHS / CA / CA97109; United States / NCRR NIH HHS / RR / P20RR021940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 5.3.4.1 / Protein Disulfide-Isomerases
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9. Radulovich N, Qian JY, Tsao MS: Human pancreatic duct epithelial cell model for KRAS transformation. Methods Enzymol; 2008;439:1-13

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  • [Title] Human pancreatic duct epithelial cell model for KRAS transformation.
  • Mutations on the KRAS gene occur early during pancreatic duct cell carcinogenesis and have been identified in up to 90% of ductal adenocarcinoma.
  • However, the functional role of KRAS mutations in the malignant transformation of normal pancreatic duct epithelial cells into cancer cells remains unknown.
  • We have developed an in vitro model for KRAS transformation using near-normal HPV-16E6E7-immortalized human pancreatic ductal epithelial (HPDE-E6E7) cells.
  • The model provides an opportunity to dissect further the molecular and cellular mechanisms associated with human pancreatic duct cell carcinogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Pancreatic Ducts / cytology. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / physiology. ras Proteins / genetics. ras Proteins / physiology
  • [MeSH-minor] Cell Culture Techniques / methods. Epithelial Cells / physiology. Genes, ras / physiology. Humans

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  • (PMID = 18374152.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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10. Agbunag C, Lee KE, Buontempo S, Bar-Sagi D: Pancreatic duct epithelial cell isolation and cultivation in two-dimensional and three-dimensional culture systems. Methods Enzymol; 2006;407:703-10
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  • [Title] Pancreatic duct epithelial cell isolation and cultivation in two-dimensional and three-dimensional culture systems.
  • Pancreatic ductal adenocarcinoma (PDA) is generally considered to have originated from pancreatic duct epithelial cells (PDEC).
  • The availability of these culture systems should be particularly useful for studying their relationships between specific genetic lesions and the morphogenic changes that accompany pancreatic ductal tumorigenesis.
  • [MeSH-major] Cell Culture Techniques / methods. Pancreatic Ducts / cytology
  • [MeSH-minor] Animals. Cell Separation. Epithelial Cells / cytology. Fluorescent Antibody Technique. Mice. Rats

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  • (PMID = 16757363.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Linder S, Myrvold K, Falkmer UG, Qvigstad G, Waldum HL, Falkmer SE: Neuroendocrine cells in pancreatic duct adenocarcinoma: an immunohistochemical study. J Exp Clin Cancer Res; 2006 Jun;25(2):213-21
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  • [Title] Neuroendocrine cells in pancreatic duct adenocarcinoma: an immunohistochemical study.
  • Pancreatic ductal adenocarcinomas can display disseminated neuroendocrine (NE) cells.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Neurosecretory Systems / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Differentiation. Cell Proliferation. Chromogranin A. Chromogranins / metabolism. Female. Humans. Immunoenzyme Techniques. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16918133.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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12. Vosters O, Beuneu C, Goldman M, Verhasselt V: N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells. Pancreas; 2008 May;36(4):363-8
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  • [Title] N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells.
  • OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion.
  • In this article, we investigated whether a salt derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement.
  • METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line.
  • To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction.
  • CONCLUSIONS: Our data suggest that Nacystelyn could be considered as a useful tool to prevent immune and inflammatory responses in pancreatic disorders by interfering with the CD40 pathway in pancreatic duct cells.
  • [MeSH-major] Acetylcysteine / analogs & derivatives. Acetylcysteine / pharmacology. Antigens, CD40 / antagonists & inhibitors. Antigens, CD40 / genetics. Inflammation / prevention & control. Lysine / analogs & derivatives. Pancreatic Ducts / physiopathology
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. NF-kappa B / drug effects. NF-kappa B / genetics. Pancreatic Neoplasms / pathology. Transcription, Genetic / drug effects

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  • (PMID = 18437082.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / N-acetylcysteine lysinate; 0 / NF-kappa B; K3Z4F929H6 / Lysine; WYQ7N0BPYC / Acetylcysteine
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13. Shimizu K, Kitahashi T, Fujii H, Tsutsumi M, Mori T, Honoki K, Tsujiuchi T: Alterations in the Smad4 gene in hamster pancreatic duct adenocarcinomas and established cell lines. Oncol Rep; 2006 Jul;16(1):85-9

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  • [Title] Alterations in the Smad4 gene in hamster pancreatic duct adenocarcinomas and established cell lines.
  • Alterations of the Smad4 gene, identified as a mediator of the transforming growth factor-beta pathway, were investigated in hamster pancreatic duct adenocarcinomas (PDAs) and established cell lines.
  • A total of 12 PDAs obtained 10 weeks after beginning the experiment and three cell lines established from subcutaneously transplantable PDAs in syngeneic hamsters were examined for mutations using reverse transcription-polymerase chain reaction-single strand conformation polymorphism (RT-PCR-SSCP) analysis.
  • A mutation was detected in only one PDA (1/12, 8.3%) in the form of an ACC to ATC (Thr to IIe) transition at codon 73; none were detected in the three cell lines.
  • These results suggest that the Smad4 gene might play a role in limited fraction of BOP-induced pancreatic duct carcinogenesis in hamsters.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Pancreatic Ductal / genetics. Gene Expression Regulation, Neoplastic. Smad4 Protein / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cricetinae. Female. Genetic Predisposition to Disease. Mesocricetus. Nitrosamines. Polymorphism, Single-Stranded Conformational. RNA / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16786127.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Nitrosamines; 0 / Smad4 Protein; 60599-38-4 / nitrosobis(2-oxopropyl)amine; 63231-63-0 / RNA
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14. Martínez-Romero C, Rooman I, Skoudy A, Guerra C, Molero X, González A, Iglesias M, Lobato T, Bosch A, Barbacid M, Real FX, Hernández-Muñoz I: The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma. J Pathol; 2009 Oct;219(2):205-13
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  • [Title] The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma.
  • Chronic pancreatitis and pancreatic ductal adenocarcinoma (PDAC) are associated with major changes in cell differentiation.
  • Polycomb proteins are epigenetic silencers expressed in adult stem cells; up-regulation of Polycomb proteins has been reported to occur in a variety of solid tumours such as colon and breast cancer.
  • We hypothesized that Polycomb might play a role in preneoplastic states in the pancreas and in tumour development/progression.
  • To test these ideas, we determined the expression of PRC1 complex proteins (Bmi1 and Ring1b) during pancreatic development and in pancreatic tissue from mouse models of disease: acute and chronic pancreatic injury, duct ligation, and in K-Ras(G12V) conditional knock-in and caerulein-treated K-Ras(G12V) mice.
  • The study was extended to human pancreatic tissue samples.
  • To obtain mechanistic insights, Bmi1 expression in cells undergoing in vitro exocrine cell metaplasia and the effects of Bmi1 depletion in an acinar cancer cell line were studied.
  • We found that Bmi1 and Ring1B are expressed in pancreatic exocrine precursor cells during early development and in ductal and islet cells-but not acinar cells-in the adult pancreas.
  • Bmi1 expression was induced in acinar cells during acute injury, in acinar-ductal metaplastic lesions, as well as in pancreatic intraepithelial neoplasia (PanIN) and PDAC.
  • Our results suggest that Bmi1 and Ring1B are modulated in pancreatic diseases and could contribute differently to tumour development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Nuclear Proteins / metabolism. Pancreatic Neoplasms / metabolism. Pancreatitis, Chronic / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cells, Cultured. Disease Models, Animal. Humans. Male. Metaplasia / metabolism. Mice. Mice, Inbred C57BL. Pancreas / metabolism. Pancreas, Exocrine / metabolism. Pancreas, Exocrine / pathology. Pancreatitis / metabolism. Polycomb Repressive Complex 1. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Wistar. Transcription Factors / metabolism

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  • [Copyright] 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 19585519.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Bmi1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / transcription factor PTF1; EC 6.3.2.19 / Polycomb Repressive Complex 1
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15. Askari MD, Tsao MS, Cekanova M, Schuller HM: Ethanol and the tobacco-specific carcinogen, NNK, contribute to signaling in immortalized human pancreatic duct epithelial cells. Pancreas; 2006 Jul;33(1):53-62
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  • [Title] Ethanol and the tobacco-specific carcinogen, NNK, contribute to signaling in immortalized human pancreatic duct epithelial cells.
  • OBJECTIVES: Smoking is a well-documented risk factor for pancreatic cancer.
  • The tobacco-specific nitrosamine, NNK (4-[methylnitrosamino]-1-[3-pyridyl]-1-butanone), significantly induces pancreatic ductal adenocarcinomas in laboratory rodents.
  • Ethanol consumption is associated with the development of chronic pancreatitis, also considered a predisposing factor for pancreatic ductal adenocarcinoma.
  • Because the precise role of ethanol in pancreatic carcinogenesis is not known, this study sought to elucidate the cumulative effects of ethanol and NNK on particular signal transduction pathways that might play a role in cell proliferation in immortalized human pancreatic duct epithelial cells.
  • METHODS: The HPDE6-c7 cells are developed from pancreatic duct epithelial cells, which are the putative cells of origin of pancreatic ductal adenocarcinoma.
  • Cell proliferation assays, Western blot, and cyclic adenosine monophosphate assays were used to demonstrate the effects of ethanol and NNK treatments on these cells.
  • CONCLUSIONS: These findings suggest a potential role for these pathways contributing to the development of smoking- and alcohol-related pancreatic carcinogenesis.
  • [MeSH-major] Carcinogens / toxicity. Cell Transformation, Neoplastic / drug effects. Ethanol / toxicity. Nitrosamines / toxicity. Pancreatic Ducts / drug effects. Signal Transduction
  • [MeSH-minor] CREB-Binding Protein / metabolism. Cell Line. Cell Proliferation. Cocarcinogenesis. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation

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  • (PMID = 16804413.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Carcinogens; 0 / Nitrosamines; 3K9958V90M / Ethanol; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; E0399OZS9N / Cyclic AMP; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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16. Omura N, Li CP, Li A, Hong SM, Walter K, Jimeno A, Hidalgo M, Goggins M: Genome-wide profiling of methylated promoters in pancreatic adenocarcinoma. Cancer Biol Ther; 2008 Jul;7(7):1146-56
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  • [Title] Genome-wide profiling of methylated promoters in pancreatic adenocarcinoma.
  • RESULTS: 1,010 of 87,922 probes on the 88 K promoter array (606 genes) had a higher signal (log(2) > 2) in the pancreatic cancer line, Panc-1 compared to the non-neoplastic pancreatic duct line, HPDE.
  • More than 1/2 of the genes aberrantly hypermethylated in Panc-1 were not expressed in the pancreatic duct (HPDE) by expression array analysis.
  • Using the 244 K CpG island array, 1,968 CpG islands were differentially methylated in MiaPaca2 compared to normal pancreas.
  • Analysis of 57 pancreatic cancers and 34 normal pancreata using MSP identified MDFI, hsa-miR-9-1, ZNF415, CNTNAP2 and ELOVL4 as methylated in 96%, 89%, 86%, 82% and 68% of the cancers vs. 9%, 15%, 6%, 3% and 97% of normal pancreata, respectively.
  • METHODS: We used methylated CpG island amplification (MCA) and Agilent promoter and CpG island microarrays to identify differential DNA methylation patterns in pancreatic cancer vs. normal pancreas.
  • CONCLUSION: Promoter and CpG island array analysis finds aberrant methylation of hundreds of promoters and CpG islands in pancreatic cancer cells.

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  • [CommentIn] Cancer Biol Ther. 2008 Jul;7(7):1157-9 [18698160.001]
  • (PMID = 18535405.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA062924-090008; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA062924-130008; United States / NCI NIH HHS / CA / CA062924-110008; United States / NCI NIH HHS / CA / P50 CA062924-120008; United States / NCI NIH HHS / CA / P50 CA062924-100008; United States / NCI NIH HHS / CA / P50 CA062924-090008; United States / NCI NIH HHS / CA / CA062924-120008; United States / NCI NIH HHS / CA / P50 CA062924-130008; United States / NCI NIH HHS / CA / P50 CA062924-110008; United States / NCI NIH HHS / CA / CA062924-100008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS107839; NLM/ PMC2763640
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17. Geismann C, Morscheck M, Koch D, Bergmann F, Ungefroren H, Arlt A, Tsao MS, Bachem MG, Altevogt P, Sipos B, Fölsch UR, Schäfer H, Müerköster SS: Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer. Cancer Res; 2009 May 15;69(10):4517-26
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  • [Title] Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer.
  • Pancreatic ductal adenocarcinoma (PDAC) is thought to originate from ductal structures, exhibiting strong desmoplastic reaction with stromal pancreatic myofibroblasts (PMF), which are supposed to drive PDAC tumorigenesis.
  • Thus, this study aimed to investigate whether PMFs are involved in the induction of tumoral L1CAM and whether this contributes to malignant transformation of pancreatic ductal cells and PDAC tumorigenesis.
  • Immunohistochemistry of tissues from chronic pancreatitis specimens revealed considerable L1CAM expression in ductal structures surrounded by dense fibrotic tissue, whereas no L1CAM staining was seen in normal pancreatic tissues.
  • Using the human pancreatic duct cell line H6c7, we show that coculture with PMFs led to a transforming growth factor-beta1 (TGF-beta1)-dependent up-regulation of L1CAM expression.
  • This mechanism of TGF-beta1-induced L1CAM expression and the resulting phenotype could be verified in the TGF-beta1-responsive PDAC cell lines Colo357 and Panc1.
  • Our data provide new insights into the mechanisms of tumoral L1CAM induction and how PMFs contribute to malignant transformation of pancreatic duct cells early in PDAC tumorigenesis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Neural Cell Adhesion Molecule L1 / genetics. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Transcription Factors / physiology. Transforming Growth Factor beta1 / physiology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. Cell Line. Cell Line, Tumor. Cell Movement. Cell Transformation, Neoplastic. Coculture Techniques. Humans. Mice. Pancreatitis / pathology. Pancreatitis / surgery. RNA, Small Interfering / genetics. Transfection. Up-Regulation

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  • (PMID = 19435915.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecule L1; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / snail family transcription factors
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18. Cavallari I, Silic-Benussi M, Rende F, Martines A, Fogar P, Basso D, Vella MD, Pedrazzoli S, Herman JG, Chieco-Bianchi L, Esposito G, Ciminale V, D'Agostino DM: Decreased expression and promoter methylation of the menin tumor suppressor in pancreatic ductal adenocarcinoma. Genes Chromosomes Cancer; 2009 May;48(5):383-96
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  • [Title] Decreased expression and promoter methylation of the menin tumor suppressor in pancreatic ductal adenocarcinoma.
  • Loss of menin, a tumor suppressor coded by the MEN1 gene, is a key factor in the pathogenesis of multiple endocrine neoplasia type I and in a percentage of sporadic endocrine tumors of the pancreas and parathyroid glands.
  • This study investigated expression of the menin protein in the normal exocrine pancreas and in pancreatic ductal adenocarcinoma (PDAC), the most common pancreatic tumor.
  • Immunofluorescence (IF) analyses showed that menin is expressed at high levels in normal acinar and duct cells.
  • IF analyses also revealed low to undetectable menin expression in the PDAC cell lines MiaPaCa-2 and Panc-1.
  • Ectopic expression of menin in these cells resulted in a marked alteration of the cell cycle, with an increase in the G1/S+G2 ratio.
  • These findings represent the first evidence that the MEN1 gene is a target of mutation and methylation in PDAC and that menin influences the cell cycle profile of duct cells.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Aged. Base Sequence. Cell Cycle. Cell Line, Tumor. Epigenesis, Genetic. Female. Fluorescent Antibody Technique. Humans. Loss of Heterozygosity. Male. Middle Aged. Molecular Sequence Data. Multivariate Analysis. Pancreas, Exocrine / cytology. Pancreas, Exocrine / metabolism. Pancreatic Ducts / cytology. Pancreatic Ducts / metabolism. Polymerase Chain Reaction. Proportional Hazards Models

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  • [Copyright] Copyright 2009 Wiley-Liss,Inc.
  • (PMID = 19170121.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
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19. Haas SL, Jesnowski R, Steiner M, Hummel F, Ringel J, Burstein C, Nizze H, Liebe S, Löhr JM: Expression of tissue factor in pancreatic adenocarcinoma is associated with activation of coagulation. World J Gastroenterol; 2006 Aug 14;12(30):4843-9
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  • [Title] Expression of tissue factor in pancreatic adenocarcinoma is associated with activation of coagulation.
  • AIM: To study expression of tissue factor (TF) in pancreatic cancer and its role in the development of thromboembolism.
  • METHODS: TF expression was studied in eight human pancreatic carcinoma cell lines by Northern blot and indirect immunofluorescence.
  • In addition, TF expression was determined by immunofluorescence in pancreatic tissues of 19 patients with pancreatic adenocarcinoma (PCa), 9 patients with chronic pancreatitis (CP) and 20 normal controls.
  • RESULTS: All pancreatic carcinoma cell lines expressed TF (8/8) and most of them expressed asTF (6/8).
  • TF expression at the protein level did not correlate with the differentiation of the carcinoma cell line.
  • All but two pancreatic cancer tissue samples stained positive for TF (17/19).
  • In all samples of CP weak staining was restricted to pancreatic duct cells, whereas only a few subendothelial cells were positive in 9/20 of normal controls.
  • CONCLUSION: We conclude that in addition to the upregulated expression of TF on the cell membrane, soluble TF might contribute to activation of the coagulation system in pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Blood Coagulation. Pancreatic Neoplasms / metabolism. Thromboembolism / metabolism. Thromboplastin / metabolism
  • [MeSH-minor] Aged. Cell Line, Tumor. Female. Humans. Male. Middle Aged

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  • (PMID = 16937466.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 9035-58-9 / Thromboplastin
  • [Other-IDs] NLM/ PMC4087618
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20. Askari MD, Tsao MS, Schuller HM: The tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone stimulates proliferation of immortalized human pancreatic duct epithelia through beta-adrenergic transactivation of EGF receptors. J Cancer Res Clin Oncol; 2005 Oct;131(10):639-48
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  • [Title] The tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone stimulates proliferation of immortalized human pancreatic duct epithelia through beta-adrenergic transactivation of EGF receptors.
  • PURPOSE: Pancreatic ductal adenocarcinoma is an aggressive smoking-associated human cancer in both men and women.
  • Binding of NNK to these receptors stimulates proliferation of pulmonary and pancreatic adenocarcinomas cells in vitro and in hamster models.
  • The goal of this study was to elucidate the NNK effects on the signal transduction pathways downstream of both beta(1)- and beta(2)-adrenergic receptors in immortalized human pancreatic HPDE6-c7 cells.
  • METHODS: The HPDE6-c7 cells are developed from normal pancreatic duct epithelial cells which are the putative cells of origin of pancreatic ductal adenocarcinoma.
  • 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT) cell proliferation assays, Western blot and cyclic AMP assays were employed to demonstrate the effects of NNK and other beta(1)- and beta(2)-adrenergic agonists and antagonist treatments on these cells.
  • RESULTS: MTT cell proliferation assays demonstrated that NNK and the classic beta-adrenergic agonist, isoproterenol, increased cell proliferation in HPDE6-c7 cells.
  • CONCLUSION: These findings suggest that the NNK -mediated beta-adrenergic receptor transactivation of the EGFR and phosphorylation of Erk1/2 in immortalized human pancreatic duct epithelial cells as a novel mechanism might contribute to the development of tobacco-associated pancreatic carcinogenesis.
  • [MeSH-major] Carcinogens / pharmacology. Cell Proliferation / drug effects. Epithelium / drug effects. Nitrosamines / pharmacology. Receptors, Adrenergic, beta-2 / drug effects
  • [MeSH-minor] Adrenergic beta-Agonists / pharmacology. Blotting, Western. Carcinoma, Pancreatic Ductal / etiology. Cell Line, Transformed. Cyclic AMP / metabolism. Humans. Isoproterenol / pharmacology. Mitogen-Activated Protein Kinase Kinases / drug effects. Mitogen-Activated Protein Kinase Kinases / metabolism. Pancreatic Ducts / drug effects. Pancreatic Neoplasms / etiology. Phosphorylation. Receptor, Epidermal Growth Factor / drug effects. Receptor, Epidermal Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Signal Transduction / physiology. Tobacco / adverse effects. Tobacco / chemistry. Transcriptional Activation / drug effects

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  • (PMID = 16091975.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Carcinogens; 0 / Nitrosamines; 0 / Receptors, Adrenergic, beta-2; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; E0399OZS9N / Cyclic AMP; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; L628TT009W / Isoproterenol
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21. Lisovsky M, Dresser K, Woda B, Mino-Kenudson M: Immunohistochemistry for cell polarity protein lethal giant larvae 2 differentiates pancreatic intraepithelial neoplasia-3 and ductal adenocarcinoma of the pancreas from lower-grade pancreatic intraepithelial neoplasias. Hum Pathol; 2010 Jun;41(6):902-9
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  • [Title] Immunohistochemistry for cell polarity protein lethal giant larvae 2 differentiates pancreatic intraepithelial neoplasia-3 and ductal adenocarcinoma of the pancreas from lower-grade pancreatic intraepithelial neoplasias.
  • Pancreatic intraepithelial neoplasia is a precursor to ductal adenocarcinoma of the pancreas that shows gastric differentiation.
  • Pancreatic intraepithelial neoplasia-3 has the highest potential to progress to adenocarcinoma, and its distinction from lower-grade pancreatic intraepithelial neoplasias is important for clinical management.
  • However, morphologic grading of pancreatic intraepithelial neoplasia suffers from significant interobserver variability.
  • A product of cell polarity gene lethal giant larvae 2 is a marker of gastric foveolar epithelium expressed in a basolateral fashion, which is lost or mislocalized in gastric epithelial dysplasia and adenocarcinoma.
  • In this study, we investigated a role of lethal giant larvae 2 expression in differentiating low-grade pancreatic intraepithelial neoplasias, that is, pancreatic intraepithelial neoplasia-1 and pancreatic intraepithelial neoplasia-2, from pancreatic intraepithelial neoplasia-3 and pancreatic ductal adenocarcinoma.
  • The immunohistochemical patterns of lethal giant larvae 2 expression were examined in normal pancreatic ducts, 48 pancreatic intraepithelial neoplasia lesions of all histologic grades, and 91 adenocarcinomas on a tissue microarray or conventional sections.
  • Whereas normal duct epithelia did not exhibit lethal giant larvae immunoreactivity, all but one lesion of low-grade pancreatic intraepithelial neoplasia showed basolateral lethal giant larvae staining.
  • Conversely, all lesions of pancreatic intraepithelial neoplasia-3 and adenocarcinoma showed loss of lethal giant larvae 2 staining and/or its cytoplasmic localization.
  • In conclusion, our results show that low-grade pancreatic intraepithelial neoplasias express lethal giant larvae 2 in a basolateral fashion recapitulating expression in normal gastric epithelium.
  • Loss or abnormal lethal giant larvae 2 expression is seen in pancreatic intraepithelial neoplasia-3 and adenocarcinoma and might be useful in separating them from lower-grade pancreatic intraepithelial neoplasias.
  • [MeSH-major] Carcinoma in Situ / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Cytoskeletal Proteins / biosynthesis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Cell Polarity. Diagnosis, Differential. Gastric Mucosa / metabolism. Humans. Immunohistochemistry. Pancreas / metabolism. Pancreas / pathology

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20233622.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Hugl-2 protein, human
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22. Nobili C, Degrate L, Caprotti R, Franciosi C, Leone BE, Trezzi R, Romano F, Uggeri F, Uggeri F: Prolonged survival of a patient affected by pancreatic adenocarcinoma with massive lymphocyte and dendritic cell infiltration after interleukin-2 immunotherapy. Report of a case. Tumori; 2008 May-Jun;94(3):426-30
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  • [Title] Prolonged survival of a patient affected by pancreatic adenocarcinoma with massive lymphocyte and dendritic cell infiltration after interleukin-2 immunotherapy. Report of a case.
  • Several studies have shown that there is a paucity of immune cells within the stroma of pancreatic adenocarcinoma, a very aggressive cancer with a median survival of about 18 months.
  • Abdominal ultrasound revealed intra- and extrahepatic bile duct dilatation and a 45-mm diameter hypoechoic solid mass within the pancreatic head; a computed tomography scan excluded vascular infiltration and metastatic lesions.
  • Histopathology showed G3 pancreatic ductal adenocarcinoma infiltrating the anterior and posterior peripancreatic tissue, duodenal wall and intrapancreatic common bile duct, with sarcoma-like foci and a component of intraductal tumor involving the common bile duct.
  • In the distal pancreas, widespread foci of pancreatic intraepithelial neoplasia (PanI2-3) were found.
  • Sections were immunostained for the T-lymphocyte marker CD3 and for the dendritic cell marker CD1a.
  • Preoperative immunotherapy with interleukin-2 may contribute to massive stromal infiltration of immune cells in pancreatic adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / therapeutic use. Dendritic Cells. Interleukin-2 / therapeutic use. Lymphocytes. Neoadjuvant Therapy / methods. Pancreatic Neoplasms / pathology. Pancreaticoduodenectomy

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  • (PMID = 18705415.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-2
  • [Number-of-references] 32
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23. Shimamura T, Royal RE, Kioi M, Nakajima A, Husain SR, Puri RK: Interleukin-4 cytotoxin therapy synergizes with gemcitabine in a mouse model of pancreatic ductal adenocarcinoma. Cancer Res; 2007 Oct 15;67(20):9903-12
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  • [Title] Interleukin-4 cytotoxin therapy synergizes with gemcitabine in a mouse model of pancreatic ductal adenocarcinoma.
  • Targeting cell surface receptors with cytotoxins or immunotoxins provides a unique opportunity for tumor therapy.
  • Here, we show the efficacy of the combination therapy of gemcitabine with an interleukin-4 (IL-4) cytotoxin composed of IL-4 and truncated Pseudomonas exotoxin in animal models of pancreatic ductal adenocarcinoma (PDA).
  • We have observed that 42 of 70 (60%) tumor samples from patients with PDA express moderate- to high-density surface IL-4 receptor (IL-4R), whereas normal pancreatic samples express no or low-density IL-4R.
  • IL-4 cytotoxin was specifically and highly cytotoxic [50% protein synthesis inhibition (IC50) ranging from >0.1 to 13 ng/mL] to six of eight pancreatic cancer cell lines, whereas no cytotoxicity (IC50>1,000 ng/mL) was observed in normal human pancreatic duct epithelium cells, fibroblasts, and human umbilical vein endothelial cells (HUVEC).
  • To confirm synergistic antitumor activity in vivo and monitor precise real-time disease progression, we used a novel metastatic and orthotopic mouse model using green fluorescent protein-transfected cancer cells and whole-body imaging system.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Deoxycytidine / analogs & derivatives. Interleukin-4 / administration & dosage. Interleukin-4 / metabolism. Leukocidins / administration & dosage. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Synergism. Green Fluorescent Proteins / genetics. Humans. Mice. Mice, Nude. Receptors, Interleukin-4 / biosynthesis. Receptors, Interleukin-4 / metabolism. Recombinant Fusion Proteins / administration & dosage. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 17942922.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Receptors, Interleukin-4; 0 / Recombinant Fusion Proteins; 0W860991D6 / Deoxycytidine; 147336-22-9 / Green Fluorescent Proteins; 207137-56-2 / Interleukin-4; B76N6SBZ8R / gemcitabine
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24. Jesnowski R, Zubakov D, Faissner R, Ringel J, Hoheisel JD, Lösel R, Schnölzer M, Löhr M: Genes and proteins differentially expressed during in vitro malignant transformation of bovine pancreatic duct cells. Neoplasia; 2007 Feb;9(2):136-46
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  • [Title] Genes and proteins differentially expressed during in vitro malignant transformation of bovine pancreatic duct cells.
  • Pancreatic carcinoma has an extremely bad prognosis due to lack of early diagnostic markers and lack of effective therapeutic strategies.
  • Recently, we have established an in vitro model recapitulating the first steps in the carcinogenesis of the pancreas.
  • SV40 large T antigen-immortalized bovine pancreatic duct cells formed intrapancreatic adenocarcinoma tumors on k-ras(mut) transfection after orthotopic injection in the nude mouse pancreas.
  • Differential expression was verified for some of the genes or proteins in samples from pancreatic carcinoma.
  • Among these genes and proteins, the majority had already been described either to be influenced by a mutated ras or to be differentially expressed in pancreatic adenocarcinoma, thus proving the feasibility of our model.
  • Other genes and proteins (e.g., BBC1, GLTSCR2, and rhoGDIalpha), up to now, have not been implicated in pancreatic tumor development.
  • Thus, we were able to establish an in vitro model of pancreatic carcinogenesis, which enabled us to identify genes and proteins differentially expressed during the early steps of malignant transformation.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Cell Transformation, Neoplastic / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / biosynthesis. Pancreatic Ducts / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Animals. Antigens, Polyomavirus Transforming / physiology. Cattle. Cell Line, Transformed / metabolism. Cell Transformation, Viral / genetics. Chronic Disease. Disease Progression. Electrophoresis, Gel, Two-Dimensional. Genes, ras. Humans. Oligonucleotide Array Sequence Analysis. Pancreatitis / genetics. Pancreatitis / metabolism. Polymerase Chain Reaction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Subtraction Technique

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  • (PMID = 17356710.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC1819583
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25. Ogata S, Kimura A, Hatsuse K, Yamamoto J, Shimazaki H, Nakanishi K, Kawai T: Poorly differentiated adenocarcinoma with signet-ring cell carcinoma of the extrahepatic bile duct in a 42-year-old Japanese female: a case report. Acta Med Okayama; 2010 Feb;64(1):63-5
MedlinePlus Health Information. consumer health - Bile Duct Cancer.

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  • [Title] Poorly differentiated adenocarcinoma with signet-ring cell carcinoma of the extrahepatic bile duct in a 42-year-old Japanese female: a case report.
  • Poorly differentiated adenocarcinoma without papilla or tubule formation of the extrahepatic bile duct is rare.
  • Imaging studies revealed a bile duct tumor obstructing the common bile duct and invading the surrounding tissues.
  • Pathologic examination revealed a dense periductal growth of poorly differentiated adenocarcinoma containing signet-ring cells, but without papilla or tubule formation in the extrahepatic bile duct.
  • The tumor cells directly invaded the pancreatic parenchyma and the portal vein.
  • In the extrahepatic bile duct, poorly differentiated adenocarcinoma may be established as a distinct clinicopathologic entity if the tumors are characterized by:.
  • [MeSH-major] Adenocarcinoma / pathology. Bile Duct Neoplasms / pathology. Bile Ducts, Extrahepatic / pathology. Carcinoma, Signet Ring Cell / pathology

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  • (PMID = 20200586.001).
  • [ISSN] 0386-300X
  • [Journal-full-title] Acta medica Okayama
  • [ISO-abbreviation] Acta Med. Okayama
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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26. Al-Wadei HA, Majidi M, Tsao MS, Schuller HM: Low concentrations of beta-carotene stimulate the proliferation of human pancreatic duct epithelial cells in a PKA-dependent manner. Cancer Genomics Proteomics; 2007 Jan-Feb;4(1):35-42
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  • [Title] Low concentrations of beta-carotene stimulate the proliferation of human pancreatic duct epithelial cells in a PKA-dependent manner.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is among the most common causes of cancer death.
  • While some of the preclinical data suggested cancer preventive effects of these agents, they have disappointed in clinical investigations.
  • MATERIALS AND METHODS: The effects of low concentrations (10 fM-200 nM)of beta-carotene on the proliferation, intracellular cAMP levels, PKA activation status and phosphorylation of EGFR-specific tyrosine kinases and ERK1/2 in immortalized human pancreatic duct epithelial cells was investigated.
  • Our data indicate that low concentrations of beta-carotene stimulate the proliferation of the putative origin of PDAC, pancreatic duct epithelial cells via cAMP and PKA-dependent transactivation of the EGFR pathway.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinases / metabolism. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Pancreatic Ducts / cytology. Pancreatic Ducts / drug effects. beta Carotene / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Colforsin / pharmacology. Enzyme Activation / drug effects. Enzyme Induction / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / biosynthesis. Mitogen-Activated Protein Kinase 3 / biosynthesis. Phosphorylation / drug effects. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 17726239.001).
  • [ISSN] 1109-6535
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA42829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 01YAE03M7J / beta Carotene; 1F7A44V6OU / Colforsin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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27. Pryczynicz A, Guzińska-Ustymowicz K, Kemona A, Czyzewska J: Expression of the E-cadherin-catenin complex in patients with pancreatic ductal adenocarcinoma. Folia Histochem Cytobiol; 2010 Jan 1;48(1):128-33
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  • [Title] Expression of the E-cadherin-catenin complex in patients with pancreatic ductal adenocarcinoma.
  • Changes in their expression and functioning reflect invasive and metastatic properties of cancer cells.
  • The study objective was to assess changes in the expressions of E-cadherin and alpha-, beta- and gamma-catenin proteins in pancreatic duct carcinoma in correlation with clinicopathological parameters, lymph node involvement and distant metastases.
  • Twenty-nine patients with pancreatic duct carcinoma were analyzed in relation to gender and age, histological type, histological malignancy grade (G), local lymph node involvement and distant metastases.
  • Reduced expression or abnormal localization of E-cadherin and alpha-, beta- and gamma-catenins were observed in pancreatic duct carcinoma.

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  • (PMID = 20529828.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / CDH1 protein, human; 0 / Cadherins; 0 / Catenins; 0 / alpha Catenin; 0 / beta Catenin; 0 / gamma Catenin
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28. Iwamuro M, Kubota J, Saito S, Goubaru M, Ohta T, Ogata M, Takuma Y, Tanaka S, Makino Y, Murakami I: [A case of mixed duct-islet cell tumor of the pancreas]. Nihon Shokakibyo Gakkai Zasshi; 2007 Jun;104(6):829-36
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  • [Title] [A case of mixed duct-islet cell tumor of the pancreas].
  • The tumor on the pancreatic body of 22 mm size was revealed by close inspection, and was diagnosed as insulinoma.
  • Surgical resection was performed, but curative resection was impossible because the component of adenocarcinoma infiltrating into surrounding tissue coexisted with insulinoma.
  • Postoperatively, we make a diagnosis of combined tumor of the pancreas, i.e. mixed duct-islet cell carcinoma.
  • [MeSH-major] Carcinoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Insulinoma / diagnosis. Neoplasms, Multiple Primary. Pancreatic Neoplasms / diagnosis

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  • (PMID = 17548951.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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29. Ringel J, Jesnowski R, Moniaux N, Lüttges J, Ringel J, Choudhury A, Batra SK, Klöppel G, Löhr M: Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma. Cancer Res; 2006 Sep 15;66(18):9045-53
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  • [Title] Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma.
  • To understand the role of ADAM17/tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) in pancreatic ductal adenocarcinoma (PDAC), we investigated its expression, function, and in vitro regulation.
  • ADAM17/TACE mRNA was expressed in 3 of 10 normal pancreatic tissues, 6 of 8 samples from patients with chronic pancreatitis, 10 of 10 PDAC tissues, and 9 of 9 pancreatic cancer cell lines, but it was absent in primary duct epithelial cells.
  • Immunohistochemical staining revealed positive cancer cells in 8 of 10 PDACs but no staining of ducts in normal pancreas.
  • ADAM17/TACE was found in 0 of 16 pancreatic intraepithelial neoplasia (PanIN)-1A lesions, 1 of 30 PanIN-1B lesions, 2 of 13 PanIN-2 lesions but, in 13 of 15 PanIN-3 lesions, associated with PDAC.
  • Western blot, flow cytometry, and confocal microscopy analyses showed the aberrant expression of ADAM17/TACE protein in pancreatic cancer cell lines.
  • Furthermore, ADAM17/TACE mRNA expression was down-regulated in pancreatic cancer cells arrested in G2-M phase as well as in a time-dependent manner after TNF-alpha and interleukin-6 incubation.
  • [MeSH-major] ADAM Proteins / biosynthesis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Cycle / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Neoplasm Invasiveness. Pancreatitis, Chronic / enzymology. Pancreatitis, Chronic / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16982746.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA772712
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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30. Löhr M, Klöppel G, Maisonneuve P, Lowenfels AB, Lüttges J: Frequency of K-ras mutations in pancreatic intraductal neoplasias associated with pancreatic ductal adenocarcinoma and chronic pancreatitis: a meta-analysis. Neoplasia; 2005 Jan;7(1):17-23
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  • [Title] Frequency of K-ras mutations in pancreatic intraductal neoplasias associated with pancreatic ductal adenocarcinoma and chronic pancreatitis: a meta-analysis.
  • Molecular analyses have demonstrated mutations in the K-ras gene at codon 12 in the majority of pancreatic ductal adenocarcinomas (PDACs).
  • In order to determine whether the K-ras mutation rate increases parallel to the grade of dysplasia in duct lesions, we performed a meta-analysis of the studies published between 1988 and 2003 that provide information on K-ras mutations in hyperplastic and dysplastic duct lesions in the pancreas.
  • The described duct lesions were reclassified according to the nomenclature for pancreatic intraepithelial neoplasia (PanIN), and the molecular methods for detecting K-ras were reviewed.
  • The incidence of K-ras mutations in PanIN lesions associated with chronic pancreatitis (CP) or normal pancreas was low (around 10%).
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Genes, ras / genetics. Mutation / genetics. Pancreatic Ducts / pathology. Pancreatic Neoplasms / genetics. Pancreatitis / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Humans

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  • (PMID = 15720814.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1490318
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31. Todoroki T, Sano T, Yamada S, Hirahara N, Toda N, Tsukada K, Motojima R, Motojima T: Clear cell carcinoid tumor of the distal common bile duct. World J Surg Oncol; 2007;5:6
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  • [Title] Clear cell carcinoid tumor of the distal common bile duct.
  • BACKGROUND: Carcinoid tumors rarely arise in the extrahepatic bile duct and can be difficult to distinguish from carcinoma.
  • There are no reports of clear cell carcinoid (CCC) tumors in the distal bile duct (DBD) to the best of our knowledge.
  • Herein, we report a CCC tumor in the DBD and review the literature concerning extrahepatic bile duct carcinoid tumors.
  • Under suspicion of carcinoma, we resected the head of the pancreas along with 2nd portion duodenectomy and a lymph node dissection.
  • Immunohistochemical stains showed that neoplastic cells were positive for neuron-specific enolase (NSE), chromogranin A, synaptophysin, and pancreatic polypeptide and negative for inhibin, keratin, CD56, serotonin, gastrin and somatostatin.
  • CONCLUSION: Given the preoperative difficulty in differentiating carcinoid from carcinoma, the pancreaticoduodenectomy is an appropriate treatment choice for carcinoid tumors located within the intra-pancreatic bile duct.
  • [MeSH-major] Carcinoid Tumor / diagnosis. Carcinoid Tumor / surgery. Common Bile Duct Neoplasms / diagnosis. Common Bile Duct Neoplasms / surgery. Pancreaticoduodenectomy / methods
  • [MeSH-minor] Adenocarcinoma, Clear Cell / diagnosis. Adenocarcinoma, Clear Cell / pathology. Adenocarcinoma, Clear Cell / surgery. Aged. Biopsy, Needle. Cholangiopancreatography, Endoscopic Retrograde. Cholangiopancreatography, Magnetic Resonance. Follow-Up Studies. Humans. Immunohistochemistry. Laparotomy / methods. Male. Neoplasm Staging. Risk Assessment. Tomography, X-Ray Computed. Treatment Outcome. Ultrasonography, Doppler

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  • (PMID = 17227590.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 52
  • [Other-IDs] NLM/ PMC1785380
  • [General-notes] NLM/ Original DateCompleted: 20070802
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32. Hruban RH, Maitra A, Kern SE, Goggins M: Precursors to pancreatic cancer. Gastroenterol Clin North Am; 2007 Dec;36(4):831-49, vi
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  • [Title] Precursors to pancreatic cancer.
  • Infiltrating ductal adenocarcinoma of the pancreas is believed to arise from morphologically distinct noninvasive precursor lesions.
  • These precursors include the intraductal papillary mucinous neoplasm, the mucinous cystic neoplasm, and pancreatic intraepithelial neoplasia.
  • Intraductal papillary mucinous neoplasms are grossly visible mucin-producing epithelial neoplasms that arise in the main pancreatic duct or one of its branches.
  • The cysts of mucinous cystic neoplasms do not communicate with the major pancreatic ducts, and these neoplasms are characterized by a distinct ovarian-type stroma.
  • Pancreatic intraepithelial neoplasia is a microscopic lesion.

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  • (PMID = 17996793.001).
  • [ISSN] 0889-8553
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062924-130011; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA062924-130011
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 103
  • [Other-IDs] NLM/ NIHMS35907; NLM/ PMC2194627
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33. Kubota K, Kakuta Y, Inayama Y, Yoneda M, Abe Y, Inamori M, Kirikoshi H, Saito S, Nakajima A, Sugimori K, Matuo K, Kazunaga T, Shimada H: Clinicopathologic study of resected cases of primary carcinoma of the cystic duct. Hepatogastroenterology; 2008 Jul-Aug;55(85):1174-8
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  • [Title] Clinicopathologic study of resected cases of primary carcinoma of the cystic duct.
  • BACKGROUND/AIMS: There have been few reports of primary carcinoma of the cystic duct (CCD) included in advanced cases.
  • METHODOLOGY: Six cases of CCD were diagnosed in which the main carcinomatous component arose from the cystic bile duct, even if these carcinomas were accompanied by invasion beyond the cystic duct.
  • Histopathologic findings (i.e., H.E. staining and cell proliferating potency assessed by ki-67 staining) were compared between the main lesion and invasive lesion of the CCD.
  • Direct cholangiography demonstrated unilateral obstruction of the common bile duct in 4 out of the 6 cases.
  • Histopathological study revealed papillary and/or well differentiated adenocarcinoma in the cases where the lesion predominantly involved the cystic duct, whereas those lesions which extended beyond the cystic duct were composed of moderate and/or poorly differentiated tubular adenocarcinoma.
  • CONCLUSIONS: CCD showed the hepatic hilum and/or confluence pattern of invasion when the tumor extended beyond the cystic duct.
  • CCD extending beyond the cystic duct was associated with more aggressive characteristics of the tumors, with perineural infiltration and histopathologic features resembling those of pancreatic cancer.
  • It is concluded that CCDs extending beyond the cystic duct are more aggressive and associated with a poorer prognosis.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Bile Duct Neoplasms / surgery. Carcinoma / pathology. Carcinoma / surgery. Cystic Duct

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  • (PMID = 18795652.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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34. Alldinger I, Dittert D, Peiper M, Fusco A, Chiappetta G, Staub E, Lohr M, Jesnowski R, Baretton G, Ockert D, Saeger HD, Grützmann R, Pilarsky C: Gene expression analysis of pancreatic cell lines reveals genes overexpressed in pancreatic cancer. Pancreatology; 2005;5(4-5):370-9
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  • [Title] Gene expression analysis of pancreatic cell lines reveals genes overexpressed in pancreatic cancer.
  • BACKGROUND: Pancreatic cancer is one of the leading causes of cancer-related death.
  • Using DNA gene expression analysis based on a custom made Affymetrix cancer array, we investigated the expression pattern of both primary and established pancreatic carcinoma cell lines.
  • METHODS: We analyzed the gene expression of 5 established pancreatic cancer cell lines (AsPC-1, BxPC-3, Capan-1, Capan-2 and HPAF II) and 5 primary isolates, 1 of them derived from benign pancreatic duct cells.
  • RESULTS: Out of 1,540 genes which were expressed in at least 3 experiments, we found 122 genes upregulated and 18 downregulated in tumor cell lines compared to benign cells with a fold change >3.
  • Several of the upregulated genes (like Prefoldin 5, ADAM9 and E-cadherin) have been associated with pancreatic cancer before.
  • The other differentially regulated genes, however, play a so far unknown role in the course of human pancreatic carcinoma.
  • By means of immunohistochemistry we could show that thymosin beta-10 (TMSB10), upregulated in tumor cell lines, is expressed in human pancreatic carcinoma, but not in non-neoplastic pancreatic tissue, suggesting a role for TMSB10 in the carcinogenesis of pancreatic carcinoma.
  • CONCLUSION: Using gene expression profiling of pancreatic cell lines we were able to identify genes differentially expressed in pancreatic adenocarcinoma, which might contribute to pancreatic cancer development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Down-Regulation. Gene Expression Profiling. Pancreatic Neoplasms / genetics. Up-Regulation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Male. Middle Aged. Pancreas / metabolism. Thymosin / genetics. Thymosin / metabolism

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  • [Copyright] Copyright 2005 S. Karger AG, Basel.
  • (PMID = 15983444.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 61512-21-8 / Thymosin; 87397-91-9 / thymosin beta(10)
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35. Katayama M, Funakoshi A, Sumii T, Sanzen N, Sekiguchi K: Laminin gamma2-chain fragment circulating level increases in patients with metastatic pancreatic ductal cell adenocarcinomas. Cancer Lett; 2005 Jul 8;225(1):167-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laminin gamma2-chain fragment circulating level increases in patients with metastatic pancreatic ductal cell adenocarcinomas.
  • Laminin-5 (LN5) is expressed solely by epithelial cells and considered to enhance cell migration after being cleaved by proteases, leading to the shedding of the N-terminal fragment of the LN5 gamma2-chain (G2F).
  • The G2F level in pancreatic ductal cell adenocarcinoma patients with liver metastases was markedly elevated, but that in patients without liver metastases was not significantly elevated.
  • The G2F levels in patients with benign pancreatic tumours (pancreatic cysts and intraductal papillary mucinous tumours) were similar to that in healthy volunteers.
  • Interestingly, a significant increase in circulating G2F/G1F ratio was observed in patients with bile duct and gallbladder carcinoma, as well as in those with metastatic pancreatic ductal cell adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Cell Adhesion Molecules / blood. Laminin / blood. Liver Neoplasms / secondary. Neoplasm Metastasis. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology

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  • (PMID = 15922869.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / LAMC2 protein, human; 0 / Laminin; 0 / kalinin
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36. Plentz R, Park JS, Rhim AD, Abravanel D, Hezel AF, Sharma SV, Gurumurthy S, Deshpande V, Kenific C, Settleman J, Majumder PK, Stanger BZ, Bardeesy N: Inhibition of gamma-secretase activity inhibits tumor progression in a mouse model of pancreatic ductal adenocarcinoma. Gastroenterology; 2009 May;136(5):1741-9.e6
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  • [Title] Inhibition of gamma-secretase activity inhibits tumor progression in a mouse model of pancreatic ductal adenocarcinoma.
  • BACKGROUND & AIMS: The Notch signaling pathway is required for the expansion of undifferentiated pancreatic progenitor cells during embryonic development and has been implicated in the progression of pancreatic ductal adenocarcinoma (PDAC).
  • METHODS: We tested the effects of a gamma-secretase inhibitor (GSI) that blocks Notch signaling in PDAC cell lines and a genetically engineered mouse model of PDAC (Kras p53 L/+ mice).
  • The GSI inhibited the growth of premalignant pancreatic duct-derived cells in a Notch-dependent manner.
  • Additionally, in a panel of over 400 human solid tumor-derived cell lines, PDAC cells, as a group, were more sensitive to the GSI than any other tumor type.

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  • (PMID = 19208345.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5P01CA117969; United States / NCI NIH HHS / CA / 5K01CA104647; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / R01 CA133557; United States / NIDDK NIH HHS / DK / T32-DK007066; United States / NIDDK NIH HHS / DK / T32 DK007066
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic S-Oxides; 0 / MRK 003; 0 / Receptors, Notch; 0 / Thiadiazoles; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS88478; NLM/ PMC3675892
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37. Adachi T, Tajima Y, Kuroki T, Mishima T, Kitasato A, Fukuda K, Tsutsumi R, Kanematsu T: Bile-reflux into the pancreatic ducts is associated with the development of intraductal papillary carcinoma in hamsters. J Surg Res; 2006 Nov;136(1):106-11
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] Bile-reflux into the pancreatic ducts is associated with the development of intraductal papillary carcinoma in hamsters.
  • BACKGROUND: Reflux of pancreatic juice into the biliary tract is a well-known risk factor for the development of biliary carcinoma.
  • In this study, we investigated the significance of bile-reflux into the pancreatic ducts in pancreatic carcinogenesis, especially in the development of carcinoma in the main pancreatic duct in hamsters.
  • MATERIALS AND METHODS: Syrian hamsters were subjected to three different surgical procedures: cholecystoduodenostomy with dissection of the extrahepatic bile duct on the distal end of the common duct (Model A); cholecystoduodenostomy along with a dissection of the common bile duct (Model B); or simple laparotomy (Model C).
  • RESULTS: Pancreas carcinomas developed in 95, 88, and 90% of the Model A hamsters (n = 22), B (n = 24), and C (n = 21), respectively.
  • The induced pancreatic tumors were histologically classified into four types: papillary; tubular; cystic adenocarcinoma; or intraductal carcinoma of the main pancreatic duct consisting of intraductal papillary carcinoma (IPC) and intraductal tubular carcinoma (ITC).
  • Bile-reflux into the pancreatic ducts was clearly demonstrated in only hamsters of Model A by means of Indocyanine green injection via the portal vein.
  • Proliferative cell nuclear antigen labeling indices of the epithelial cells in the main pancreatic duct in hamsters, with no BOP treatment, were 3.8, 0.8, and 1.1% in Models A (n = 10), B (n = 10), and C (n = 10), respectively, and the difference was statistically significant (P < 0.01).
  • CONCLUSIONS: Our findings suggest that bile-reflux into the pancreatic ducts is a significant factor predisposing to the development of IPC of the pancreas through an acceleration of epithelial cell kinetics of the main pancreatic duct.
  • [MeSH-major] Adenocarcinoma / etiology. Bile Reflux / complications. Carcinoma, Pancreatic Ductal / etiology. Carcinoma, Papillary / etiology. Pancreatic Neoplasms / etiology
  • [MeSH-minor] Animals. Bile Acids and Salts / metabolism. Carcinogens. Cell Division. Cholecystostomy. Common Bile Duct / surgery. Cricetinae. Disease Models, Animal. Duodenostomy. Epithelial Cells / pathology. Female. Mesocricetus. Nitrosamines. Pancreatic Ducts / pathology. Proliferating Cell Nuclear Antigen / metabolism. Sphincter of Oddi Dysfunction / complications. Sphincter of Oddi Dysfunction / metabolism

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  • (PMID = 16863651.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Carcinogens; 0 / Nitrosamines; 0 / Proliferating Cell Nuclear Antigen; 60599-38-4 / nitrosobis(2-oxopropyl)amine
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38. Oshiro H, Matsuo K, Mawatari H, Inayama Y, Yamanaka S, Nagahama K, Endo I, Shimada H, Nakajima A, Kubota K: Mucin-producing gallbladder adenocarcinoma with focal small cell and large cell neuroendocrine differentiation associated with pancreaticobiliary maljunction. Pathol Int; 2008 Dec;58(12):780-6
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  • [Title] Mucin-producing gallbladder adenocarcinoma with focal small cell and large cell neuroendocrine differentiation associated with pancreaticobiliary maljunction.
  • Although the patient's status and laboratory data initially suggested biliary pancreatitis due to gallstone, radiography and endoscopy confirmed the presence of pancreaticobiliary maljunction and a gallbladder tumor with excessive mucin, in which the duodenal papilla and the common bile duct were impacted.
  • Additionally, small foci of small cell and large cell neuroendocrine carcinomatous components were observed.
  • Thus, the final classification of pT2N0M0 stage II was given to this lesion, according to the Union Internationale Contre le Cancer guidelines.
  • [MeSH-major] Adenocarcinoma / pathology. Common Bile Duct / abnormalities. Gallbladder Neoplasms / pathology. Mucins / metabolism. Pancreatic Ducts / abnormalities

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  • (PMID = 19067853.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
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39. Seeley ES, Carrière C, Goetze T, Longnecker DS, Korc M: Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia. Cancer Res; 2009 Jan 15;69(2):422-30
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  • [Title] Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia.
  • In this study, we determined that ciliogenesis is suppressed in both pancreatic cancer cells and pancreatic intraepithelial neoplasia (PanIN) lesions in human pancreatic ductal adenocarcinoma (PDAC).
  • Inhibition of Kras effector pathways restored ciliogenesis in a mouse pancreatic cancer cell line, raising the possibility that ciliogenesis may be actively repressed by oncogenic Kras.
  • By contrast, normal duct, islet, and centroacinar cells retained primary cilia in both human and mouse pancreata.

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  • (PMID = 19147554.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102687-05; United States / NCI NIH HHS / CA / CA-102687; United States / NCI NIH HHS / CA / R01 CA102687; United States / NCI NIH HHS / CA / CA-127095; United States / NCI NIH HHS / CA / R01 CA102687-05; United States / NCI NIH HHS / CA / CA-101306; United States / NCI NIH HHS / CA / R21 CA127095; United States / NCI NIH HHS / CA / R01 CA075059; United States / NCI NIH HHS / CA / CA101306-05; United States / NCI NIH HHS / CA / R01 CA101306; United States / NCI NIH HHS / CA / R01 CA101306-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS79339; NLM/ PMC2629528
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40. Bickenbach K, Galka E, Roggin KK: Molecular mechanisms of cholangiocarcinogenesis: are biliary intraepithelial neoplasia and intraductal papillary neoplasms of the bile duct precursors to cholangiocarcinoma? Surg Oncol Clin N Am; 2009 Apr;18(2):215-24, vii
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  • [Title] Molecular mechanisms of cholangiocarcinogenesis: are biliary intraepithelial neoplasia and intraductal papillary neoplasms of the bile duct precursors to cholangiocarcinoma?
  • Although the key steps of cholangiocarcinogenesis remain unknown, it has been hypothesized that CC may develop through two key premalignant precursor lesions: biliary intraepithelial neoplasia (BilIN) and intraductal papillary neoplasm of the bile duct (IPNB).
  • These lesions probably are analogous to pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm, respectively.
  • It highlights the genetic mutations that alter cellular proliferation, tumor suppression, and impairment of critical mucinous, cell-adhesion, and matrix proteins.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic / pathology. Cholangiocarcinoma / pathology. Precancerous Conditions / pathology

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  • (PMID = 19306808.001).
  • [ISSN] 1055-3207
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
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41. Satoh K, Hamada S, Kanno A, Hirota M, Umino J, Ito H, Masamune A, Egawa S, Unno M, Shimosegawa T: Expression of MSX2 predicts malignancy of branch duct intraductal papillary mucinous neoplasm of the pancreas. J Gastroenterol; 2010 Jul;45(7):763-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of MSX2 predicts malignancy of branch duct intraductal papillary mucinous neoplasm of the pancreas.
  • BACKGROUND: To distinguish malignant from benign branch duct (BD)-intraductal papillary mucinous neoplasm (IPMN) still remains difficult.
  • Recently, we revealed that MSX2 was frequently expressed in pancreatic cancer and its expression was correlated with aggressive behavior of the cancer.
  • The role of MSX2 in the pancreatic duct cell was assessed by the induced expression of MSX2 in a normal human pancreatic duct epithelial cell line (HPDE).
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Papillary / genetics. Homeodomain Proteins / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / pathology. Aged. Cell Line. Cell Proliferation. Epithelial Cells / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Multivariate Analysis. Pancreatic Ducts / cytology. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology. Predictive Value of Tests. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20107842.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MSX2 protein; 0 / RNA, Messenger
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42. Hashimoto Y, Murakami Y, Uemura K, Hayashidani Y, Sudo T, Ohge H, Fukuda E, Sueda T, Hiyama E: Detection of human telomerase reverse transcriptase (hTERT) expression in tissue and pancreatic juice from pancreatic cancer. Surgery; 2008 Jan;143(1):113-25
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of human telomerase reverse transcriptase (hTERT) expression in tissue and pancreatic juice from pancreatic cancer.
  • BACKGROUND: Human telomerase reverse transcriptase (hTERT), a catalytic subunit of telomerase, is a promising diagnostic candidate for pancreatic cancer.
  • To evaluate the feasibility of immunohistochemistry (IHC) for the diagnosis of pancreatic cancer, hTERT expression and telomerase activity were assayed in pancreatic tissues, ex vivo brushing, and pancreatic juice samples with various pancreatic diseases.
  • METHODS: Telomerase activity was analyzed using the TRAP assay and hTERT was examined by IHC in 85 pancreatic tumor samples, 17 ex vivo pancreatic duct brushings, and 27 pancreatic juice samples.
  • In pancreatic juice samples, 10 of 11 IDCs and 3 of 4 malignant IPMNs expressed hTERT, in which seven samples were not diagnosed as malignant on cytologic exam.
  • The diagnoses of pancreatic cancer based on hTERT IHC exhibited high rates of sensitivity (87%), specificity (92%), and overall accuracy (89%), whereas the sensitivity of cytologic examination was 53%.
  • CONCLUSIONS: Our results suggested that hTERT expression in epithelia indicates malignant transformation in pancreatic tumors and immunohistochemical detection of hTERT in cells derived from pancreatic juice provides a potent method for cancer diagnosis.
  • [MeSH-major] Pancreatic Juice / chemistry. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / diagnosis. Telomerase / analysis
  • [MeSH-minor] Adenocarcinoma, Mucinous / chemistry. Adult. Aged. Aged, 80 and over. Carcinoma, Pancreatic Ductal / chemistry. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / chemistry. Cell Line, Tumor. Chronic Disease. Feasibility Studies. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Pancreatitis / metabolism. Sensitivity and Specificity

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  • (PMID = 18154939.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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43. Sadakari Y, Ienaga J, Kobayashi K, Miyasaka Y, Takahata S, Nakamura M, Mizumoto K, Tanaka M: Cyst size indicates malignant transformation in branch duct intraductal papillary mucinous neoplasm of the pancreas without mural nodules. Pancreas; 2010 Mar;39(2):232-6
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  • [Title] Cyst size indicates malignant transformation in branch duct intraductal papillary mucinous neoplasm of the pancreas without mural nodules.
  • OBJECTIVES: In branch duct intraductal papillary mucinous neoplasm (IPMN) of the pancreas, the importance of the cyst size to predict malignancy is still controversial.
  • Our aim was to elucidate the malignant potential of branch duct IPMN without mural nodules (flat branch duct IPMN).
  • METHODS: Seventy-three patients with flat branch duct IPMNs were studied in our institution.
  • Statistically significant predictors of malignancy were atypical cytological condition and main pancreatic duct (MPD) diameter of 5 mm or more.
  • The frequency of malignancy in flat branch duct IPMNs with the size of 30 mm or more and MPD diameter of less than 5 mm was 3.6%, whereas there were 5 malignant cases (26.3%) in flat branch duct IPMNs with the size of 30 mm or more and MPD diameter of 5 mm or more.
  • CONCLUSIONS: We conclude that the size criteria (> or =30 mm) to predict malignancy proposed in the international consensus guidelines is appropriate and resection or meticulous follow-up using cytological examination and MPD dilatation is needed in patients with flat branch duct IPMNs.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Papillary / pathology. Carcinoma, Pancreatic Ductal / pathology. Cell Transformation, Neoplastic / pathology. Pancreatic Cyst / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 19752768.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Zhong L: Magnetic resonance imaging in the detection of pancreatic neoplasms. J Dig Dis; 2007 Aug;8(3):128-32
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  • [Title] Magnetic resonance imaging in the detection of pancreatic neoplasms.
  • Recently, with the rapid scanning time and improved image quality, outstanding advances in magnetic resonance (MR) methods have resulted in an increase in the use of MRI for patients with a variety of pancreatic neoplasms.
  • The non-invasive all-in-one MR multi-imaging techniques may provide the comprehensive information needed for the preoperative diagnosis and evaluation of pancreatic neoplasms.
  • Pancreatic neoplasms include primary tumors and pancreatic metastases.
  • Primary tumors of the pancreas may be mainly classified as ductal adenocarcinomas, cystic tumors and islet cell tumors (ICT).
  • Pancreatic adenocarcinomas can be diagnosed in a MRI study depending on direct evidence or both direct and indirect evidence.
  • The combined MRI features of a focal pancreatic mass, pancreatic duct dilatation and parenchymal atrophy are highly suggestive of a ductal adenocarcinoma.
  • Most cystic neoplasms of the pancreas are either microcystic adenomas or mucinous cystic neoplasms.
  • Intraductal papillary mucinous tumors are the uncommon low-grade malignancy of the pancreatic duct.
  • ICT are rare neoplasms arising from neuroendocrine cells in the pancreas or the periampullary region.
  • The most frequent tumors to metastasize to the pancreas are cancers of the breast, lung, kidney and melanoma.
  • [MeSH-major] Cholangiopancreatography, Magnetic Resonance. Magnetic Resonance Angiography. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / pathology. Humans. Neoplasms, Cystic, Mucinous, and Serous / diagnosis. Neoplasms, Cystic, Mucinous, and Serous / pathology. Pancreas / pathology

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  • (PMID = 17650223.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 10
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45. Lisovsky M, Dresser K, Baker S, Fisher A, Woda B, Banner B, Lauwers GY: Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study. Mod Pathol; 2009 Jul;22(7):977-84
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  • [Title] Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study.
  • The diagnosis of gastric epithelial dysplasia, a precursor lesion of gastric adenocarcinoma, is hindered by interobserver variability and by its resemblance to regenerative changes.
  • Loss of cell polarity, a histological feature of gastric epithelial dysplasia, may be difficult to ascertain, especially in the setting of inflammation or injury.
  • A biomarker of cell polarity could be useful in diagnosis of dysplasia, but has not been reported.
  • The goal of our study was to test the hypothesis that Lgl2 protein expression and/or localization are disrupted in gastric epithelial dysplasia and adenocarcinoma.
  • Normal esophageal, duodenal, colonic, biliary, and pancreatic duct mucosae, as well as gastric intestinal metaplasia, did not express Lgl2.
  • All but one case each of gastric epithelial dysplasia and adenocarcinoma showed either complete loss of anti-Lgl2 immunoreactivity or diffuse, mostly weak, cytoplasmic staining.
  • Our data suggest that Lgl2 expression is either aberrantly localized or lost in gastric epithelial dysplasia and adenocarcinoma, whereas it is maintained in reactive gastric mucosa.
  • We propose that Lgl2 may be a potential marker to rule out gastric epithelial dysplasia and adenocarcinoma in diagnostic specimens.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Cytoskeletal Proteins / metabolism. Gastric Mucosa / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Cell Polarity. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Male. Middle Aged. Young Adult

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  • (PMID = 19407852.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Hugl-2 protein, human
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46. Demeter I, Hegyesi O, Nagy AK, Case MR, Steward MC, Varga G, Burghardt B: Bicarbonate transport by the human pancreatic ductal cell line HPAF. Pancreas; 2009 Nov;38(8):913-20
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  • [Title] Bicarbonate transport by the human pancreatic ductal cell line HPAF.
  • OBJECTIVES: The human pancreatic duct cell line, HPAF, has been shown previously to secrete Cl(-) in response to Ca(2+)-mobilizing stimuli.
  • [MeSH-minor] 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / analogs & derivatives. 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / pharmacology. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Adenosine Triphosphate / pharmacology. Amiloride / analogs & derivatives. Amiloride / pharmacology. Biological Transport / drug effects. Bumetanide / pharmacology. Cell Line, Tumor. Chlorides / metabolism. Cytophotometry. Fluoresceins / chemistry. Humans. Hydrogen-Ion Concentration. Intracellular Space / chemistry. Ion Transport / drug effects. Membrane Potentials / drug effects. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology. Pancreatic Ducts / physiopathology. Sodium Potassium Chloride Symporter Inhibitors / pharmacology. Sodium-Potassium-Chloride Symporters / metabolism. Solute Carrier Family 12, Member 2

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  • (PMID = 19745779.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bicarbonates; 0 / Chlorides; 0 / Fluoresceins; 0 / SLC12A2 protein, human; 0 / Sodium Potassium Chloride Symporter Inhibitors; 0 / Sodium-Potassium-Chloride Symporters; 0 / Solute Carrier Family 12, Member 2; 0Y2S3XUQ5H / Bumetanide; 1154-25-2 / ethylisopropylamiloride; 61481-03-6 / dihydro-DIDS; 7DZO8EB0Z3 / Amiloride; 85138-49-4 / 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein; 8L70Q75FXE / Adenosine Triphosphate; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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47. Sano T, Shimada K, Sakamoto Y, Ojima H, Esaki M, Kosuge T: Prognosis of perihilar cholangiocarcinoma: hilar bile duct cancer versus intrahepatic cholangiocarcinoma involving the hepatic hilus. Ann Surg Oncol; 2008 Feb;15(2):590-9
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  • [Title] Prognosis of perihilar cholangiocarcinoma: hilar bile duct cancer versus intrahepatic cholangiocarcinoma involving the hepatic hilus.
  • BACKGROUND: Clinically hepatobiliary resection is indicated for both hilar bile duct cancer (BDC) and intrahepatic cholangiocarcinoma involving the hepatic hilus (CCC).
  • On multivariate analysis, three independent factors were related to longer survival in BDC patients: achieved in curative resection with cancer free margin (R0) (P = .024, odds ratio 1.862), well differentiated or papillary adenocarcinoma (P = .011, odds ratio 2.135), and absence of lymph node metastasis (P < .001, odds ratio 3.314).
  • Five factors were related to longer survival in CCC patients: absence of intrahepatic daughter nodules (P < .001, odds ratio 2.318), CEA level </=2.9 ng/mL (P = .005, odds ratio 2.606), no red blood cell transfusion requirement (P = .016, odds ratio 2.614), absence or slight degree of lymphatic system invasion (P < .001, odds ratio 4.577), and negative margin of the proximal bile duct (P = .003, odds ratio 7.398).
  • [MeSH-major] Bile Duct Neoplasms / mortality. Bile Ducts, Intrahepatic. Cholangiocarcinoma / mortality
  • [MeSH-minor] Adult. Cell Differentiation. Female. Hepatectomy. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local / mortality. Prognosis. Proportional Hazards Models. Risk Factors. Survival Analysis

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  • (PMID = 18057991.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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48. Chu PG, Schwarz RE, Lau SK, Yen Y, Weiss LM: Immunohistochemical staining in the diagnosis of pancreatobiliary and ampulla of Vater adenocarcinoma: application of CDX2, CK17, MUC1, and MUC2. Am J Surg Pathol; 2005 Mar;29(3):359-67
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  • [Title] Immunohistochemical staining in the diagnosis of pancreatobiliary and ampulla of Vater adenocarcinoma: application of CDX2, CK17, MUC1, and MUC2.
  • We studied the expression of cytokeratin 7 (CK7), cytokeratin 17 (CK17), cytokeratin 20 (CK20), CDX2, mucin 1 (MUC1), mucin 2 (MUC2), and mucin 5AC (MUC5AC) in 46 cases of pancreatic ductal carcinoma, 18 ampulla of Vater adenocarcinomas, and 24 intrahepatic cholangiocarcinomas.
  • The expression of MUC1 and CK17 was restricted to pancreatic ductal carcinoma (41 of 46, 89%; 38 of 46, 83%, respectively), the ampullary carcinoma of pancreatobiliary origin (6 of 6, 100%; 5 of 6, 83%, respectively), and intrahepatic cholangiocarcinoma (20 of 24, 83%; 17 of 24, 71%, respectively).
  • The expression of MUC2 and CDX2 was restricted to the intestinal, mucinous, and signet-ring cell-type adenocarcinomas of duodenal papillary origin (9 of 11, 82%; 11 of 11, 100%, respectively).
  • MUC2 was rarely expressed in pancreatic ductal carcinoma (1 of 46, 2%) and was negative in the ampullary carcinoma of pancreatobiliary origin and in intrahepatic cholangiocarcinoma.
  • A heterogeneous CDX2 staining pattern was seen in 1 of 6 cases of the ampullary carcinoma of pancreatobiliary origin (17%), 5 of 24 intrahepatic cholangiocarcinomas (21%), and 10 of 46 (22%) pancreatic ductal carcinomas.
  • In contrast, all 11 cases of the intestinal, mucinous, and signet-ring cell-type adenocarcinomas of duodenal papillary origin showed homogeneous CDX2 nuclear positivity.
  • MUC1+/CK17+ can be used as positive markers for pancreatic ductal carcinomas, the ampullary carcinoma of pancreatobiliary origin, and cholangiocarcinomas with positive predictive values of 76%, 83%, and 58%, respectively.
  • MUC2+/CDX2+ can be used as positive markers for the intestinal-type adenocarcinoma of duodenal papillary origin with a positive predictive value of 82%.
  • [MeSH-major] Ampulla of Vater / pathology. Bile Ducts, Intrahepatic / pathology. Carcinoma, Pancreatic Ductal / pathology. Cholangiocarcinoma / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratins / metabolism. Male. Mucins / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 15725805.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Mucins; 0 / Neoplasm Proteins; 68238-35-7 / Keratins
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49. Fong D, Steurer M, Obrist P, Barbieri V, Margreiter R, Amberger A, Laimer K, Gastl G, Tzankov A, Spizzo G: Ep-CAM expression in pancreatic and ampullary carcinomas: frequency and prognostic relevance. J Clin Pathol; 2008 Jan;61(1):31-5
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  • [Title] Ep-CAM expression in pancreatic and ampullary carcinomas: frequency and prognostic relevance.
  • AIMS: Pancreatic adenocarcinoma is an aggressive gastrointestinal malignancy with only a few long-term survivors even after radical surgery.
  • Patients with ampullary cancer have a better prognosis but adjuvant therapy needs further improvement.
  • Epithelial cell adhesion molecule (Ep-CAM) is strongly expressed in a variety of epithelial cancers and represents a promising target for immunological tumour therapy.
  • Thus, the aim of this study was to investigate Ep-CAM expression and its potential prognostic impact in pancreatic and ampullary carcinomas.
  • METHODS: Ep-CAM expression was investigated retrospectively by immunohistochemistry in paraffin-embedded primary tumour tissue samples from a series of consecutive patients with pancreatic (n = 153) and ampullary cancer (n = 34).
  • RESULTS: Ep-CAM overexpression was observed in 85 of 153 pancreatic cancer specimens (56%) and in 29 of 34 ampullary cancer samples (85%).
  • However, subgroup analyses showed that Ep-CAM overexpression correlated with shorter overall survival among patients with ampullary cancer and advanced stage pancreatic cancer.
  • Furthermore, in ampullary cancer, Ep-CAM overexpression was found to correlate with tumour stage.
  • CONCLUSIONS: Ep-CAM overexpression was detectable in the majority of cases with pancreatic and ampullary cancer.
  • [MeSH-major] Ampulla of Vater. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Cell Adhesion Molecules / metabolism. Common Bile Duct Neoplasms / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16775119.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / EPCAM protein, human; 0 / Neoplasm Proteins
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50. Lee KE, Bar-Sagi D: Oncogenic KRas suppresses inflammation-associated senescence of pancreatic ductal cells. Cancer Cell; 2010 Nov 16;18(5):448-58
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  • [Title] Oncogenic KRas suppresses inflammation-associated senescence of pancreatic ductal cells.
  • Mutational activation of KRas is the first and most frequently detected genetic lesion in pancreatic ductal adenocarcinoma (PDAC).
  • Here, we report that the endogenous expression of oncogenic KRas suppresses premature senescence in primary pancreatic duct epithelial cells (PDEC).
  • Moreover, the KRas-Twist-p16(INK4A) senescence bypass pathway is employed in vivo to prevent inflammation-associated senescence of pancreatic ductal epithelium.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 21075310.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055360; United States / NCI NIH HHS / CA / R37 CA055360; United States / NCI NIH HHS / CA / R56 CA055360; United States / NCI NIH HHS / CA / CA055360
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; 0 / Twist Transcription Factor; 136253-27-5 / Twist1 protein, mouse; EC 3.2.1.23 / beta-Galactosidase; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS249223; NLM/ PMC3397918
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51. Kashiwazaki M, Takeda Y, Hasuike Y, Masuda N, Ikenaga M, Hirao M, Fujitani K, Mishima H, Sawamura T, Nakamori S, Takeda M, Mano Y, Tsujinaka T: [A case of successful resection for recurrent intraductal papillary mucinous adenocarcinoma]. Gan To Kagaku Ryoho; 2005 Oct;32(11):1863-5
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  • [Title] [A case of successful resection for recurrent intraductal papillary mucinous adenocarcinoma].
  • Intraductal papillary-mucinous neoplasms (IPMN) of the pancreas have recently been defined and classified by the World Health Organization.
  • We report a case of a 65-year-old female who underwent surgical resection of the pancreas twice within a period of 6 months for primary and recurrent IPMN.
  • A histopathological study revealed invasive adenocarcinoma and the negative margin of the pancreatic duct.
  • Recurrent IPMN consisted of adenosquamous cell carcinoma.
  • Recurrent disease in the residual pancreas suggests that a long-term surveillance is critical.
  • [MeSH-major] Adenocarcinoma, Mucinous / surgery. Adenocarcinoma, Papillary / surgery. Pancreatic Ducts. Pancreatic Neoplasms / surgery

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  • (PMID = 16315964.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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52. Novak I, Hede SE, Hansen MR: Adenosine receptors in rat and human pancreatic ducts stimulate chloride transport. Pflugers Arch; 2008 May;456(2):437-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenosine receptors in rat and human pancreatic ducts stimulate chloride transport.
  • Previously, we have shown that pancreatic acini release adenosine triphosphate (ATP) and ATP-handling enzymes, and pancreatic ducts express various purinergic P2 receptors.
  • The aim of the present study was to establish whether pancreatic ducts also express adenosine receptors and whether these could be involved in secretory processes, which involve cystic fibrosis transmembrane regulator (CFTR) Cl- channels or Ca2+-activated Cl- channels and H(+)/HCO(-)(3) transporters.
  • Reverse transcriptase polymerase chain reaction analysis on rat pancreatic ducts and human duct cell adenocarcinoma lines showed that they express A1, A2A, A2B, and A3 receptors.
  • Real-time PCR revealed relatively low messenger RNA levels of adenosine receptors compared to beta-actin; the rank order for the receptors was A2A>A2B>or=A3>>A1 for rat pancreas and A2B>A2A>>A3>or=A1 for duct cell lines.
  • Whole-cell patch-clamp recordings on rat pancreatic ducts showed that, in about half of the recordings, adenosine depolarized the membrane voltage, and this was because of the opening of Cl- channels.
  • Using a Cl--sensitive fluorophore and single-cell imaging on duct cell lines, it was found that 58% of PANC-1 cells responded to adenosine, whereas only 9% of CFPAC-1 cells responded.
  • Adenosine elicited Ca2+ signals only in a few rat and human duct cells, which did not seem to correlate with Cl- signals.
  • A2A receptors were localized in the luminal membranes of rat pancreatic ducts, plasma membrane of many PANC-1 cells, but only a few CFPAC-1 cells.
  • Taken together, our data indicate that A2A receptors open Cl- channels in pancreatic ducts cells with functional CFTR.
  • We propose that adenosine can stimulate pancreatic secretion and, thereby, is an active player in the acini-to-duct signaling.
  • [MeSH-major] Chloride Channels / metabolism. Pancreatic Ducts / metabolism. Receptors, Purinergic P1 / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Calcium Signaling / physiology. Cell Line, Tumor. Chlorides / metabolism. Cystic Fibrosis Transmembrane Conductance Regulator / genetics. Cystic Fibrosis Transmembrane Conductance Regulator / metabolism. Epithelial Cells / cytology. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. Humans. Male. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Patch-Clamp Techniques. Rats. Rats, Wistar. Receptors, Adenosine A2 / genetics. Receptors, Adenosine A2 / metabolism

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  • (PMID = 18057956.001).
  • [ISSN] 0031-6768
  • [Journal-full-title] Pflügers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chloride Channels; 0 / Chlorides; 0 / Receptors, Adenosine A2; 0 / Receptors, Purinergic P1; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator
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53. Kimura W: Pancreatic lithiasis and intraductal papillary-mucinous neoplasm with special reference to the pathogenesis of lithiasis. J Hepatobiliary Pancreat Sci; 2010 Nov;17(6):776-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic lithiasis and intraductal papillary-mucinous neoplasm with special reference to the pathogenesis of lithiasis.
  • In pancreatic lithiasis in elderly autopsy cases, the stones are small and the pancreatic duct is changed very slightly when viewed by simple X-ray film, pancreatic ductography and gross appearance.
  • Histologically, a slight fibrous increase is seen very locally, but findings consistent with chronic pancreatitis are not found throughout the whole pancreas.
  • However, marked, diffuse and irregular dilatation of the pancreatic duct is frequently found in operative cases with chronic pancreatitis and pancreatic stones.
  • These findings show that the changes seen with aging and with chronic pancreatitis can be distinguished based on the findings of pancreatic ductography.
  • Mucin production in epithelia in intraductal papillary-mucinous neoplasm (IPMN) may not be strongly associated with the pathogenesis of pancreatic lithiasis.
  • Pancreatic lithiasis may be related to squamous cell metaplasia.
  • IPMN and dilatation of the pancreatic duct are closely associated with mucin production.
  • An increase in intraductal pressure of the pancreatic duct may be somewhat related to the mechanism of stone formation.
  • The incidental co-existence of pancreatic epithelia with pancreatic lithiasis in patients with chronic pancreatitis and the development of IPMN may also be possible.
  • IPMN and pancreatic lithiasis may be related through the mechanism(s) of their pathogenesis, their synergism and the pathogenesis of stone formation.
  • The relation between mucinous metaplasia and stone formation is slight and, therefore, there may be only a weak correlation between IPMN and pancreatic stones.
  • This may explain why there are few reports of the co-existence of IPMN and pancreatic stones (Kimura in Kan Tan Sui 58:485-492, 2009).
  • [MeSH-major] Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Papillary / diagnosis. Lithiasis / diagnosis. Pancreas. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma, Mucinous. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Pancreatitis, Chronic / diagnosis. Tomography, X-Ray Computed

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  • (PMID = 19779665.001).
  • [ISSN] 1868-6982
  • [Journal-full-title] Journal of hepato-biliary-pancreatic sciences
  • [ISO-abbreviation] J Hepatobiliary Pancreat Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
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54. Morton JP, Lewis BC: Shh signaling and pancreatic cancer: implications for therapy? Cell Cycle; 2007 Jul 1;6(13):1553-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Shh signaling and pancreatic cancer: implications for therapy?
  • Hedgehog signaling has been implicated in the development of several human cancers, including small cell lung carcinomas, medulloblastomas, basal cell carcinomas, and digestive tract tumors.
  • Elevated levels of pathway components are observed in pancreatic ductal adenocarcinoma (PDAC) precursor lesions, and these levels increase further as lesions progress to more advanced stages.
  • Yet the mechanisms by which hedgehog signaling contributes to pancreatic tumorigenesis were poorly understood.
  • We recently published results showing that activated hedgehog signaling enhances the proliferation and survival of pancreatic duct epithelial cells, the presumptive target cells for PDAC development.
  • We also demonstrated that sonic hedgehog (Shh) expression, in cooperation with loss of the Trp53 and Ink4a/Arf tumor suppressor loci, was sufficient to initiate the formation of early pancreatic lesions.
  • Furthermore, Shh signaling enhanced K-Ras-mediated pancreatic tumorigenesis and reduced the dependence of tumor cells on the sustained activation of Ras-stimulated signaling pathways.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / therapy. Hedgehog Proteins / physiology. Pancreatic Neoplasms / therapy

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  • (PMID = 17611415.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Hedgehog Proteins; 0 / SHH protein, human
  • [Number-of-references] 41
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55. Nakagohri T, Kinoshita T, Konishi M, Takahashi S, Gotohda N: Nodal involvement is strongest predictor of poor survival in patients with invasive adenocarcinoma of the head of the pancreas. Hepatogastroenterology; 2006 May-Jun;53(69):447-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nodal involvement is strongest predictor of poor survival in patients with invasive adenocarcinoma of the head of the pancreas.
  • BACKGROUND/AIMS: Pancreatic cancer is a devastating disease with an extremely poor prognosis.
  • The outcome of pancreatic head cancer after surgical resection is still difficult to predict.
  • METHODOLOGY: Between September 1992 and December 2003, 100 consecutive patients with invasive adenocarcinoma of the head of the pancreas who underwent surgical resection were retrospectively analyzed to clarify the influence of clinicopathological factors.
  • RESULTS: The overall 1-, 3-, and 5-year survival rates for the 100 patients with pancreatic head cancer were 55%, 16%, and 6%, respectively.
  • Among the 16 clinicopathologic factors, 9 were significantly associated with outcome in univariate analysis: tumor type (invasive ductal cancer), poor histological differentiation, extrapancreatic plexus invasion, bile duct invasion, duodenal invasion, intrapancreatic nerve invasion, lymphatic invasion, venous invasion, and nodal involvement.
  • CONCLUSIONS: Nodal involvement was the strongest predictor of poor survival after pancreatic resection for invasive adenocarcinoma of the head of the pancreas.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Lymph Nodes / pathology. Pancreatic Neoplasms / mortality. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Pancreatectomy. Pancreaticoduodenectomy. Predictive Value of Tests. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16795990.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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56. Lowe AW, Olsen M, Hao Y, Lee SP, Taek Lee K, Chen X, van de Rijn M, Brown PO: Gene expression patterns in pancreatic tumors, cells and tissues. PLoS One; 2007 Mar 28;2(3):e323
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression patterns in pancreatic tumors, cells and tissues.
  • BACKGROUND: Cancers of the pancreas originate from both the endocrine and exocrine elements of the organ, and represent a major cause of cancer-related death.
  • This study provides a comprehensive assessment of gene expression for pancreatic tumors, the normal pancreas, and nonneoplastic pancreatic disease.
  • METHODS/RESULTS: DNA microarrays were used to assess the gene expression for surgically derived pancreatic adenocarcinomas, islet cell tumors, and mesenchymal tumors.
  • The addition of normal pancreata, isolated islets, isolated pancreatic ducts, and pancreatic adenocarcinoma cell lines enhanced subsequent analysis by increasing the diversity in gene expression profiles obtained.
  • Similarities in gene expression support the pancreatic duct as the origin of adenocarcinomas.
  • In addition, genes highly expressed in other cancers and associated with specific signal transduction pathways were also found in pancreatic tumors.

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  • (PMID = 17389914.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077097; United States / NCI NIH HHS / CA / CA77097
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Axin Protein; 0 / DNA, Neoplasm; 0 / RNA, Neoplasm; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC1824711
  • [General-notes] NLM/ Original DateCompleted: 20070726
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57. Zhu L, Shi G, Schmidt CM, Hruban RH, Konieczny SF: Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia. Am J Pathol; 2007 Jul;171(1):263-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
  • A number of studies have shown that pancreatic ductal adenocarcinoma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
  • PanINs are thought to initiate in the small ducts of the pancreas through activating mutations in the KRAS proto-oncogene.
  • What remains unanswered is the identification of the individual cell type(s) that contributes to pancreatic ductal adenocarcinoma formation.
  • To follow the cellular and molecular changes that occur in acinar and duct cell properties on Kras(G12D) expression, we took advantage of LSL-Kras(G12D/+)/p48(Cre/+) mice, which faithfully mimic the human disease.
  • In young animals (4 weeks), the predominant cellular alteration in the exocrine pancreas was acinar metaplasia in which individual acini consisted of acinar cells and duct-like cells.

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  • (PMID = 17591971.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK55489; United States / NCI NIH HHS / CA / P50 CA62924; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Erbb2ip protein, mouse; 0 / Interferon-Stimulated Gene Factor 3, gamma Subunit; 0 / Isgf3g protein, mouse; 0 / Receptors, Notch
  • [Other-IDs] NLM/ PMC1941579
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58. Yoshida T, Shiraki N, Baba H, Goto M, Fujiwara S, Kume K, Kume S: Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas. Genes Cells; 2008 Jul;13(7):667-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas.
  • Here we analyzed the expression patterns of Eppk1 in the developing and adult pancreas in the mice.
  • In the embryonic pancreas, Eppk1+/Pdx1+ and Eppk1+/Sox9+ pancreatic progenitor cells were observed in early pancreatic epithelium.
  • Then Eppk1 expression becomes confined to Ngn3+ or Sox9+ endocrine progenitor cells, and p48+ exocrine progenitor cells, and then restricted to the duct cells and a cells at birth.
  • In the adult pancreas, Eppk1 is expressed in centroacinar cells (CACs) and in duct cells.
  • Eppk1 is observed in pancreatic intraepithelial neoplasia (PanIN), previously identified as pancreatic ductal adenocarcinoma (PDAC) precursor lesions.
  • In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an acinar cell regeneration model.
  • These results suggest that Eppk1 serves as a useful marker for detecting pancreatic progenitor cells in developing and regenerating pancreas.
  • [MeSH-major] Autoantigens / biosynthesis. Autoantigens / genetics. Gene Expression Regulation / physiology. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Regeneration / physiology
  • [MeSH-minor] Animals. Biomarkers / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Knockout. Mice, Transgenic. Stem Cells / cytology. Stem Cells / metabolism


59. Watanabe H, Okada G, Ohtsubo K, Yamaguchi Y, Mouri H, Motoo Y, Wakabayashi T, Sawabu N: Expression of mesothelin mRNA in pure pancreatic juice from patients with pancreatic carcinoma, intraductal papillary mucinous neoplasm of the pancreas, and chronic pancreatitis. Pancreas; 2005 May;30(4):349-54
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  • [Title] Expression of mesothelin mRNA in pure pancreatic juice from patients with pancreatic carcinoma, intraductal papillary mucinous neoplasm of the pancreas, and chronic pancreatitis.
  • OBJECTIVES: In the gene expression analysis of pancreatic carcinoma (PCa) using serial analysis of gene expression (SAGE) according to Ryu et al, the tag for the mesothelin mRNA transcript was present in 7 of 8 SAGE libraries derived from PCa but not in the 2 SAGE libraries derived from normal pancreatic duct epithelial cells.
  • Mesothelin mRNA expression was confirmed with in situ hybridization in all 4 resected primary PCa tumors and with RT-PCR in 18 of 20 PCa cell lines, whereas mesothelin protein expression was confirmed with immunohistochemistry in all 60 resected primary PCa tissues by Argani et al.
  • We evaluated mesothelin mRNA expression in pure pancreatic juice (PPJ) obtained from patients with PCa, chronic pancreatitis (CP), and intraductal papillary mucinous neoplasm (IPMN) of the pancreas.
  • Quantitative detection of mesothelin mRNA in PPJ may have potential diagnostic implications for pancreatic tumors.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Carcinoma, Papillary / diagnosis. Membrane Glycoproteins / genetics. Pancreatic Neoplasms / diagnosis. Pancreatitis, Chronic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Biomarkers, Tumor / genetics. Cell Line, Tumor. Female. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Molecular Sequence Data. Pancreatic Juice / physiology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15841046.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / mesothelin
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60. Neupane D, Korc M: 14-3-3sigma Modulates pancreatic cancer cell survival and invasiveness. Clin Cancer Res; 2008 Dec 1;14(23):7614-23
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  • [Title] 14-3-3sigma Modulates pancreatic cancer cell survival and invasiveness.
  • PURPOSE: The purpose of the present study was to investigate the potential role of 14-3-3sigma in pancreatic ductal adenocarcinoma (PDAC).
  • EXPERIMENTAL DESIGN: 14-3-3 isoform expression was determined by real-time quantitative PCR in laser capture normal pancreatic ductal cells and pancreatic cancer cells and in 5 pancreatic cancer cell lines.
  • RESULTS: The cancer cells in 7 PDAC samples expressed high levels of 14-3-3sigma mRNA by quantitative PCR when compared with normal pancreatic duct cells.
  • Most cell lines released detectable amount of 14-3-3sigma into conditioned medium.
  • CONCLUSIONS: 14-3-3sigma contributes to the chemoresistance of pancreatic cancer cells and exerts cell type-dependent effects on cell migration and invasion.

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  • (PMID = 19047086.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075059; United States / NCI NIH HHS / CA / CA-10130; United States / NCI NIH HHS / CA / CA101306-05; United States / NCI NIH HHS / CA / R01 CA101306; United States / NCI NIH HHS / CA / R01 CA101306-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14-3-3 Proteins
  • [Other-IDs] NLM/ NIHMS85737; NLM/ PMC3142357
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61. Farina A, Dumonceau JM, Frossard JL, Hadengue A, Hochstrasser DF, Lescuyer P: Proteomic analysis of human bile from malignant biliary stenosis induced by pancreatic cancer. J Proteome Res; 2009 Jan;8(1):159-69
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  • [Title] Proteomic analysis of human bile from malignant biliary stenosis induced by pancreatic cancer.
  • Stenosis of the common bile duct may be either due to benign (chronic pancreatitis) or malignant (cholangiocarcinoma, pancreatic adenocarcinoma) conditions.
  • To this intent, we performed a proteomic analysis of bile samples from patients having a biliary stenosis caused by pancreatic adenocarcinoma.
  • Among them, several proteins have been described as potential biomarkers of pancreatic cancer.
  • We extended our investigation by studying the expression of some of these pancreatic cancer markers in bile samples collected from patients with various etiologies of biliary stenosis including pancreatic cancer, cholangiocarcinoma, chronic pancreatitis, as well as gallstone-induced stenosis.
  • Our data showed a conspicuous overexpression of CEACAM6 and MUC1 (CA19-9) in pancreatic cancer and cholangiocarcinoma samples, according to the hypothesis that bile fluid collects cancer-associated protein leaking from the tumor microenvironment.
  • [MeSH-major] Bile / metabolism. Cholestasis / metabolism. Pancreatic Neoplasms / complications. Proteomics / methods
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, CD / biosynthesis. Biomarkers / metabolism. CA-19-9 Antigen / biosynthesis. Cell Adhesion Molecules / biosynthesis. Chromatography, Liquid / methods. Electrophoresis, Polyacrylamide Gel / methods. GPI-Linked Proteins. Humans. Mass Spectrometry / methods. Middle Aged. Mucin-1 / biosynthesis

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  • (PMID = 19055478.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / CA-19-9 Antigen; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Mucin-1
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62. Lopez-Tomassetti Fernandez EM, Luis HD, Malagon AM, Gonzalez IA, Pallares AC: Recurrence of inflammatory pseudotumor in the distal bile duct: lessons learned from a single case and reported cases. World J Gastroenterol; 2006 Jun 28;12(24):3938-43
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  • [Title] Recurrence of inflammatory pseudotumor in the distal bile duct: lessons learned from a single case and reported cases.
  • Immunohistochemical study of these lesions limited to the pancreatic head or distal bile duct seems to be compatible with those observed in a new entity called autoimmune pancreatitis, but usually intense fibrotic reaction (zonation) predominates producing a mass.
  • When this condition is limited to the pancreatic head, the common bile duct might be involved by the inflammatory process and jaundice may occur often resembling adenocarcinoma of the pancreas.
  • We have previously reported a case of IMT arising from the bile duct associated with autoimmune pancreatitis which is an extremely rare entity.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Granuloma, Plasma Cell / pathology. Neoplasm Recurrence, Local / pathology

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  • (PMID = 16804988.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
  • [Number-of-references] 52
  • [Other-IDs] NLM/ PMC4087951
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63. Westgaard A, Tafjord S, Farstad IN, Cvancarova M, Eide TJ, Mathisen O, Clausen OP, Gladhaug IP: Pancreatobiliary versus intestinal histologic type of differentiation is an independent prognostic factor in resected periampullary adenocarcinoma. BMC Cancer; 2008;8:170
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  • [Title] Pancreatobiliary versus intestinal histologic type of differentiation is an independent prognostic factor in resected periampullary adenocarcinoma.
  • BACKGROUND: Resectable adenocarcinomas in the pancreatic head, by definition "periampullary", originate from ampullary, duodenal, biliary, or ductal pancreatic epithelium.
  • The aim of the study was to determine whether the histologic type of differentiation is an independent prognostic factor in periampullary adenocarcinoma, and whether tumour origin predicts the prognosis in pancreatobiliary type carcinomas independently of resection margin involvement, tumour size, nodal involvement, perineural and vascular infiltration, and degree of differentiation.
  • CONCLUSION: Pancreatobiliary versus intestinal type of differentiation independently predicts poor prognosis after pancreaticoduodenectomy for periampullary adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Ampulla of Vater / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / mortality. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Case-Control Studies. Cell Differentiation. Common Bile Duct Neoplasms / pathology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Neoplasm Invasiveness / pathology. Pancreatectomy / methods. Pancreaticoduodenectomy / methods. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 18547417.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2430209
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64. Shi G, Zhu L, Sun Y, Bettencourt R, Damsz B, Hruban RH, Konieczny SF: Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia. Gastroenterology; 2009 Apr;136(4):1368-78
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  • [Title] Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia.
  • BACKGROUND & AIMS: Invasive pancreatic ductal adenocarcinoma is thought to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN).
  • METHODS: In this study, we examined the importance of the acinar-restricted transcription factor Mist1 to KrasG12D-induced mouse PanIN (mPanIN) formation in 3 different mouse models of pancreatic cancer.
  • RESULTS: In the absence of Mist1 (Mist1KO), KrasG12D-expressing mice exhibited severe exocrine pancreatic defects that were rescued by ectopic expression of Mist1 in acinar cells. mPanIN development was greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO acinar cells were predisposed to convert to a ductal phenotype and activate epidermal growth factor receptor (EGFR) and Notch-signaling pathways.

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  • (PMID = 19249398.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK055489-10; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA124586-02; United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK055489-10; United States / NCI NIH HHS / CA / CA124586-02; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586; United States / NCI NIH HHS / CA / CA124586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Mist1 protein, mouse; 0 / Receptors, Notch; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS182460; NLM/ PMC2845927
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65. Lipsett MA, Castellarin ML, Rosenberg L: Acinar plasticity: development of a novel in vitro model to study human acinar-to-duct-to-islet differentiation. Pancreas; 2007 May;34(4):452-7
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  • [Title] Acinar plasticity: development of a novel in vitro model to study human acinar-to-duct-to-islet differentiation.
  • OBJECTIVES: The plasticity of pancreatic tissue is demonstrated in many pancreatic diseases.
  • It has previously been shown that pancreatic islet-to-duct transformation and acinoductal metaplasia have been associated with both pancreatic regeneration and adenocarcinoma in various in vivo and in vitro settings.
  • Understanding this inherent morphogenetic plasticity of the adult pancreas could lead to new therapeutic approaches to pancreatic disease.
  • Tissue samples were then analyzed for amylase, cytokeratin 19, pancreas duodenum homeobox 1, and endocrine hormone immunoreactivity as well as dithizione positivity.
  • Addition of INGAP led to an approximately 18-fold increase in pancreas duodenum homeobox 1 immunoreactivity, although without an observed increase in insulin production as measured by dithizone positivity.
  • CONCLUSIONS: We have developed a novel in vitro model of adult human acinoductal metaplasia that will aid not only in developing new methods of expanding beta-cell mass but also provide insights into pancreatic carcinogenesis.
  • [MeSH-major] Cell Differentiation. Islets of Langerhans / pathology. Pancreatic Ducts / pathology. Regeneration
  • [MeSH-minor] Adult. Amylases / metabolism. C-Peptide / metabolism. Cell Proliferation. Cells, Cultured. Cytokines / pharmacology. Gastrins / pharmacology. Hepatocyte Growth Factor / pharmacology. Homeodomain Proteins / biosynthesis. Humans. Insulin-Secreting Cells / pathology. Keratin-19 / metabolism. Metaplasia. Pancreas / pathology. Pancreas / physiopathology. Peptide Fragments / pharmacology. Phenotype. Time Factors. Trans-Activators / biosynthesis. Up-Regulation

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  • (PMID = 17446845.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / C-Peptide; 0 / Cytokines; 0 / Gastrins; 0 / Homeodomain Proteins; 0 / INGAP peptide; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 67256-21-7 / Hepatocyte Growth Factor; EC 3.2.1.- / Amylases
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66. De La O JP, Emerson LL, Goodman JL, Froebe SC, Illum BE, Curtis AB, Murtaugh LC: Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18907-12
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  • [Title] Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia.
  • Efforts to model pancreatic cancer in mice have focused on mimicking genetic changes found in the human disease, particularly the activating KRAS mutations that occur in pancreatic tumors and their putative precursors, pancreatic intraepithelial neoplasia (PanIN).
  • The basis for this selective response is unknown, and it is similarly unknown what cell types in the mature pancreas actually contribute to PanINs.
  • One clue comes from the fact that PanINs, unlike most cells in the adult pancreas, exhibit active Notch signaling.
  • We hypothesize that Notch, which inhibits differentiation in the embryonic pancreas, contributes to PanIN formation by abrogating the normal differentiation program of tumor-initiating cells.
  • Through conditional expression in the mouse pancreas, we find dramatic synergy between activated Notch and Kras in inducing PanIN formation.
  • Furthermore, we find that Kras activation in mature acinar cells induces PanIN lesions identical to those seen upon ubiquitous Kras activation, and that Notch promotes both initiation and dysplastic progression of these acinar-derived PanINs, albeit short of invasive adenocarcinoma.
  • At the cellular level, Notch/Kras coactivation promotes rapid reprogramming of acinar cells to a duct-like phenotype, providing an explanation for how a characteristically ductal tumor can arise from nonductal acinar cells.

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  • (PMID = 19028876.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / CA123066-02; United States / NCI NIH HHS / CA / R21 CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / T32 HD007491; United States / NCI NIH HHS / CA / P30 CA042014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 094ZI81Y45 / Tamoxifen; EC 3.6.5.2 / ras Proteins
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67. Ryschich E, Huszty G, Wentzensen N, Schmidt E, Knaebel HP, Encke J, Märten A, Büchler MW, Schmidt J: Effect of Flt3 ligand gene transfer in experimental pancreatic cancer. Int J Colorectal Dis; 2007 Feb;22(2):215-23
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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  • [Title] Effect of Flt3 ligand gene transfer in experimental pancreatic cancer.
  • BACKGROUND: Fms-like tyrosine kinase 3 receptor (Flt3) is an important receptor expressed on the cell membrane of immature antigen-presenting cells.
  • The aim of the present study was to study the effect of FL gene transfer on the immune response and tumor growth in experimental pancreatic cancer.
  • Transfection efficiency of subcutaneously growing rat duct-like pancreatic cancer (DSL6A) with DOTAP-/cholesterol-based liposomes was tested using a pcDNA3.1-lacZ construct.
  • Tumor induction was achieved in Lewis rats by a subcutaneous inoculation of syngeneic pancreatic tumor cells (DSL6A).
  • [MeSH-major] Adenocarcinoma / immunology. Membrane Proteins / immunology. Pancreatic Neoplasms / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Dendritic Cells / immunology. Gene Transfer Techniques. Immunotherapy. Killer Cells, Natural / immunology. Male. Molecular Sequence Data. Neoplasms, Experimental. Rats. Rats, Inbred Lew. Sequence Analysis, DNA

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  • (PMID = 16528542.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / flt3 ligand protein
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68. Logsdon CD, Ji B: Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer. Clin Gastroenterol Hepatol; 2009 Nov;7(11 Suppl):S40-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.
  • The relationship between chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) is unclear.
  • However, it has been long thought that PDAC arises only from duct cells.
  • However, we have recently found that excessive activity within the Ras signaling pathway can lead to acinar cell death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from acinar cells through the full complement of preneoplastic (pancreatic intraepithelial neoplasia) lesions.

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  • (PMID = 19896097.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / DK052067
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 46
  • [Other-IDs] NLM/ NIHMS268542; NLM/ PMC3050544
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69. Al-Wadei HA, Al-Wadei MH, Schuller HM: Prevention of pancreatic cancer by the beta-blocker propranolol. Anticancer Drugs; 2009 Jul;20(6):477-82
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  • [Title] Prevention of pancreatic cancer by the beta-blocker propranolol.
  • Pancreatic ductal adenocarcinoma (PDAC) is among the leading causes of cancer deaths and is unresponsive to existing therapy.
  • We found that propranolol had strong cancer preventive effects in this animal model.
  • Western blots of pancreatic duct cells and PDAC cells harvested by laser capture microscopy showed significant upregulation of the alpha7 nAChR associated with significant inductions of p-CREB, p-ERK1/2, and increases in epidermal growth factor and vascular endothelial growth factor in PDAC cells of hamsters not treated with propranolol.
  • [MeSH-major] Adrenergic beta-Antagonists / therapeutic use. Anticarcinogenic Agents / therapeutic use. Carcinoma, Pancreatic Ductal / prevention & control. Pancreatic Neoplasms / prevention & control. Propranolol / therapeutic use. Receptors, Adrenergic, beta / metabolism

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  • (PMID = 19387337.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829; United States / NCI NIH HHS / CA / R01 CA042829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic beta-Antagonists; 0 / Anticarcinogenic Agents; 0 / Chrna7 protein, human; 0 / Nitrosamines; 0 / Receptors, Adrenergic, beta; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 3K9958V90M / Ethanol; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 9Y8NXQ24VQ / Propranolol; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ NIHMS380612; NLM/ PMC3366433
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70. Dowen SE, Crnogorac-Jurcevic T, Gangeswaran R, Hansen M, Eloranta JJ, Bhakta V, Brentnall TA, Lüttges J, Klöppel G, Lemoine NR: Expression of S100P and its novel binding partner S100PBPR in early pancreatic cancer. Am J Pathol; 2005 Jan;166(1):81-92
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  • [Title] Expression of S100P and its novel binding partner S100PBPR in early pancreatic cancer.
  • S100P is a member of the S100 family of calcium-binding proteins and there have been several recent reports of its overexpression in pancreatic ductal adenocarcinoma (PDAC).
  • S100PBPR was found to localize to cell nuclei where S100P is also present, and the two proteins co-immunoprecipitate.
  • By in situ hybridization, S100PBPR transcript was found in islet cells but not duct cells of the healthy pancreas.
  • Both S100P and S100PBPR were detected by quantitative real-time polymerase chain reaction in pancreatic intraepithelial neoplasia (PanIN) and PDAC samples, and in situ hybridization revealed the presence of S100PBPR transcript in malignant PDAC cells.
  • These data suggest that an interaction between S100P and S100PBPR may be involved in early pancreatic cancer.
  • [MeSH-major] Calcium-Binding Proteins / genetics. Carrier Proteins / genetics. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Base Sequence. Calcium / metabolism. Cloning, Molecular. DNA Primers. Disease Progression. Humans. In Situ Hybridization. Magnesium / metabolism. Polymerase Chain Reaction. RNA, Messenger / genetics. Transfection

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  • (PMID = 15632002.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Carrier Proteins; 0 / DNA Primers; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / S100P protein, human; 0 / S100PBP protein, human; I38ZP9992A / Magnesium; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC1602285
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71. Okamoto Y, Maeba T, Kakinoki K, Okano K, Izuishi K, Wakabayashi H, Usuki H, Suzuki Y: A patient with unresectable advanced pancreatic cancer achieving long-term survival with gemcitabine chemotherapy. World J Gastroenterol; 2008 Nov 28;14(44):6876-80
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] A patient with unresectable advanced pancreatic cancer achieving long-term survival with gemcitabine chemotherapy.
  • Abdominal computed tomography (CT) and endoscopic retrograde cholangio-pancreatography (ERCP) revealed that the density of the entire pancreas had decreased, and showed dilatation of the common bile duct (CBD) and the main pancreatic duct (MPD).
  • Pancreatic cancer was diagnosed by cytological examination analyzing the pancreatic juice obtained by ERCP.
  • The entire pancreas was a hard mass, and a needle biopsy was obtained from the head, body and tail of the pancreas.
  • These biopsies diagnosed a poorly differentiated adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / administration & dosage. Deoxycytidine / analogs & derivatives. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Cell Differentiation. Chemotherapy, Adjuvant. Cholangiopancreatography, Endoscopic Retrograde. Digestive System Surgical Procedures. Drug Administration Schedule. Female. Humans. Time Factors. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19058319.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ PMC4988355
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72. Yamaguchi T, Takahashi H, Kagawa R, Takeda R, Sakata S, Yamamoto M, Nishizaki D: Huge pseudocyst of the pancreas caused by poorly differentiated invasive ductal adenocarcinoma with osteoclast-like giant cells: report of a case. Hepatogastroenterology; 2007 Mar;54(74):599-601
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] Huge pseudocyst of the pancreas caused by poorly differentiated invasive ductal adenocarcinoma with osteoclast-like giant cells: report of a case.
  • Under the tentative diagnosis of pancreatic pseudocyst of 22cm in diameter, a percutaneous drainage was performed.
  • At this time, abdominal computed tomography scan showed a tumor at the uncinate process of the pancreas.
  • It was histologically proven to be poorly differentiated ductal adenocarcinoma in combination with osteoclast-like giant cells.
  • The pseudocyst was considered to be due to the stenosis of the main pancreatic duct caused by carcinoma of the uncinate process.
  • Osteoclast-like giant cell tumor is a very rare neoplasm, the origin and prognosis of which still remain obscure.
  • However, it has to be considered in the differential diagnosis of cystic changes of the pancreas, especially of pseudocyst.
  • Furthermore, detailed surveys are needed in cases of pseudocyst of the pancreas without chronic pancreatitis, in order to identify small carcinoma of the pancreas.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / complications. Giant Cells. Osteoclasts. Pancreatic Neoplasms / complications. Pancreatic Pseudocyst / etiology
  • [MeSH-minor] Aged. Amylases / blood. Biomarkers, Tumor / blood. Cholangiopancreatography, Endoscopic Retrograde. Cholestasis, Extrahepatic / complications. Cholestasis, Extrahepatic / diagnosis. Cholestasis, Extrahepatic / pathology. Cholestasis, Extrahepatic / surgery. Decompression, Surgical. Diagnosis, Differential. Fatal Outcome. Follow-Up Studies. Humans. Liver Function Tests. Male. Pancreas / pathology. Pancreatectomy. Pancreatic Function Tests. Pancreatitis, Chronic / complications. Pancreatitis, Chronic / diagnosis. Pancreatitis, Chronic / pathology. Pancreatitis, Chronic / surgery. Splenectomy. Suction. Tomography, X-Ray Computed

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  • (PMID = 17523330.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.2.1.- / Amylases
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73. Johnson SK, Dennis RA, Barone GW, Lamps LW, Haun RS: Differential expression of insulin-like growth factor binding protein-5 in pancreatic adenocarcinomas: identification using DNA microarray. Mol Carcinog; 2006 Nov;45(11):814-27
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  • [Title] Differential expression of insulin-like growth factor binding protein-5 in pancreatic adenocarcinomas: identification using DNA microarray.
  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by its aggressiveness and resistance to both radiation and chemotherapeutic treatment.
  • To better understand the molecular pathogenesis of pancreatic cancer, DNA array technology was employed to identify genes differentially expressed in pancreatic tumors when compared to non-malignant pancreatic tissues.
  • RNA isolated from 11 PDACs and 14 non-malignant bulk pancreatic duct specimens was used to probe Affymetrix U95A DNA arrays.
  • The majority of the 150 genes identified have not been previously reported to be differentially expressed in pancreatic tumors, although a number of the upregulated transcripts have been reported previously.
  • Immunohistochemistry was used to correlate calponin and insulin-like growth factor binding protein-5 (IGFBP-5) RNA levels with protein expression in PDACs and revealed peritumoral calponin staining in the reactive stroma and intense focal staining of islets cells expressing IGFBP-5 at the edge of tumors; thus implicating the interplay of various cell types to promote neoplastic cell growth within pancreatic carcinomas.
  • As a potential modulator of cell proliferation, the overexpression of IGFBP-5 may, therefore, play a significant role in the malignant transformation of normal pancreatic epithelial cells.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Expression Profiling. Insulin-Like Growth Factor Binding Protein 5 / genetics. Oligonucleotide Array Sequence Analysis. Pancreatic Neoplasms / genetics

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  • (PMID = 16865675.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR-16460
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Insulin-Like Growth Factor Binding Protein 5; 0 / Microfilament Proteins; 0 / calponin
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74. Kasuya K, Nagakawa Y, Matsudo T, Ozawa T, Tsuchida A, Aoki T, Itoi T, Itokawa F: p53 gene mutation and p53 protein overexpression in a patient with simultaneous double cancer of the gallbladder and bile duct associated with pancreaticobiliary maljunction. J Hepatobiliary Pancreat Surg; 2009;16(3):376-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p53 gene mutation and p53 protein overexpression in a patient with simultaneous double cancer of the gallbladder and bile duct associated with pancreaticobiliary maljunction.
  • Pancreaticobiliary maljunction (PBM) is associated with the occurrence of biliary cancer due to pancreatobiliary reflux.
  • We present a case of simultaneous double cancer of the gallbladder and bile duct.
  • A 77-year-old woman who had jaundice, intra- and extra-hepatic biliary ductal dilatation and a space-occupying lesion in the gallbladder and lower bile duct underwent pancreatoduodenectomy.
  • The gallbladder cancer showed papillary carcinoma without mutation of the K-ras gene and with p53 non-sense mutation of CCA (Pro) to CA (Stop) on codon 301 in exon 8.
  • The bile duct cancer revealed a well-differentiated adenocarcinoma without mutation of the K-ras gene and with p53 miss-sense mutation of GTG (Val) to GAG (Glu) on codon 272 in exon 8.
  • In contrast, only the mucosa of the common channel had p53 protein accumulation and high cell proliferation activity.
  • Therefore, the genetic pathway might be the same in both the gallbladder and bile duct cancer, and a high potential for carcinogenesis might be present in the epithelium of the common channel in patients with PBM.
  • [MeSH-major] Bile Duct Neoplasms / genetics. Bile Ducts / abnormalities. Gallbladder Neoplasms / genetics. Genes, p53 / genetics. Neoplasms, Multiple Primary / genetics. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Aged. Biopsy, Needle. Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. Carcinoma, Papillary / surgery. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Genes, ras / genetics. Humans. Immunohistochemistry. Mutation, Missense. Pancreatic Ducts / abnormalities. Pancreaticoduodenectomy / methods. Polymerase Chain Reaction. Risk Assessment. Treatment Outcome

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  • (PMID = 19183832.001).
  • [ISSN] 1436-0691
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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75. Li M, Bharadwaj U, Zhang R, Zhang S, Mu H, Fisher WE, Brunicardi FC, Chen C, Yao Q: Mesothelin is a malignant factor and therapeutic vaccine target for pancreatic cancer. Mol Cancer Ther; 2008 Feb;7(2):286-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesothelin is a malignant factor and therapeutic vaccine target for pancreatic cancer.
  • Given the high fatality rate of pancreatic cancer, an effective treatment for this devastating disease is urgently needed.
  • We have shown that mesothelin expression was higher in human pancreatic cancer cells than in human pancreatic duct epithelial cells, and mesothelin mRNA was substantially overexpressed in 18 of 21 (86%) clinical pancreatic adenocarcinoma specimens when compared with the surrounding normal tissues.
  • Here we studied the effects of mesothelin overexpression in pancreatic cancer cell proliferation and migration in vitro and pancreatic cancer progression in vivo.
  • We found that forced expression of mesothelin significantly increased tumor cell proliferation and migration by 90% and 300%, respectively, and increased tumor volume by 4-fold in the nude mice xenograft model when compared with the vector control cell line.
  • Silencing of mesothelin inhibited cell proliferation and migration in pancreatic cancer cells and ablated tumor progression in vivo.
  • This study revealed novel functions of mesothelin and suggested a new therapeutic vaccine strategy whereby mesothelin is targeted to control pancreatic cancer progression.

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  • (PMID = 18281514.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / R21 AT003094-01; United States / NIDCR NIH HHS / DE / DE15542; United States / NIDCR NIH HHS / DE / DE015543-02; United States / NIDCR NIH HHS / DE / R01 DE015543; United States / NIDCR NIH HHS / DE / R01 DE015543-02; United States / NCCIH NIH HHS / AT / AT003094; United States / NCCIH NIH HHS / AT / R21 AT003094; United States / NCCIH NIH HHS / AT / AT003094-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 0 / mesothelin
  • [Other-IDs] NLM/ NIHMS228173; NLM/ PMC2929838
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76. Lee KM, Yasuda H, Hollingsworth MA, Ouellette MM: Notch 2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells. Lab Invest; 2005 Aug;85(8):1003-12
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  • [Title] Notch 2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells.
  • Pancreatic adenocarcinomas display foci of duct-like structures that are positive for markers of pancreatic ductal cells.
  • To create an in vitro system to study pancreatic adenocarcinomas, we had used an hTERT cDNA to immortalize primary cells of the human pancreas.
  • In this report, we show that the immortalized cells, termed hTERT-HPNE cells, have the ability to differentiate to pancreatic ductal cells.
  • Exposing hTERT-HPNE cells to sodium butyrate and 5-aza-2'-deoxycytidine lead to the formation of pancreatic ductal cells marked by the expression of MDR-1, carbonic anhydrase II, and the cytokeratins 7, 8, and 19. hTERT-HPNE cells were found to have properties of the intermediary cells formed during acinar-to-ductal metaplasia, which included their undifferentiated phenotype, expression of Nestin, evidence of active Notch signaling, and ability to differentiate to pancreatic ductal cells.
  • These results provide further evidence for the presence in the adult pancreas of a precursor of ductal cells. hTERT-HPNE cells should provide a useful model to study acinar-to-ductal metaplasia and the role played by this process in pancreatic cancer development.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Differentiation / physiology. Pancreas / cytology. Pancreatic Neoplasms / pathology. Receptors, Cell Surface / physiology. Stem Cells / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Line, Transformed. DNA Primers. Fluorescent Antibody Technique. Humans. Receptor, Notch2. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

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  • (PMID = 15924149.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / NOTCH2 protein, human; 0 / Receptor, Notch2; 0 / Receptors, Cell Surface
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77. Westgaard A, Schjølberg AR, Cvancarova M, Eide TJ, Clausen OP, Gladhaug IP: Differentiation markers in pancreatic head adenocarcinomas: MUC1 and MUC4 expression indicates poor prognosis in pancreatobiliary differentiated tumours. Histopathology; 2009 Feb;54(3):337-47
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  • [Title] Differentiation markers in pancreatic head adenocarcinomas: MUC1 and MUC4 expression indicates poor prognosis in pancreatobiliary differentiated tumours.
  • AIMS: To examine how accurately immunohistochemical markers discriminate between pancreatobiliary and intestinal-type adenocarcinomas in the pancreatic head and to explore the prognostic importance of these markers among each of these histological types.
  • CONCLUSIONS: Agreement between immunohistochemical and morphological classification of pancreatic head adenocarcinomas is moderate.
  • [MeSH-major] Adenocarcinoma / pathology. Antigens, Differentiation / metabolism. Bile Duct Neoplasms / pathology. Mucin-1 / metabolism. Mucin-4 / metabolism. Pancreatic Neoplasms / pathology


78. Corbo V, Ritelli R, Barbi S, Funel N, Campani D, Bardelli A, Scarpa A: Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas. PLoS One; 2010;5(9):e12653
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  • [Title] Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas.
  • Tumours of the pancreas are aggressive neoplasms for which no effective therapeutic strategy is currently available.
  • METHODOLOGY/PRINCIPAL FINDINGS: We conducted a DNA-sequence analysis of a selected set of 35 kinase genes in a panel of 52 pancreatic exocrine neoplasms, including 36 pancreatic ductal adenocarcinoma, and 16 ampulla of Vater cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Common Bile Duct Neoplasms / genetics. Mutation. Pancreatic Neoplasms / genetics. Protein Kinases / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Ampulla of Vater / enzymology. Base Sequence. Cell Line, Tumor. Female. Humans. Male. Middle Aged. Molecular Sequence Data


79. Erkan M, Kleeff J, Esposito I, Giese T, Ketterer K, Büchler MW, Giese NA, Friess H: Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis. Oncogene; 2005 Jun 23;24(27):4421-32
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  • [Title] Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis.
  • Altered expression of apoptosis-regulating genes plays an important role in the aggressive growth behavior and chemoresistance of pancreatic ductal adenocarcinoma.
  • In the present study, the hypoxia-inducible proapoptotic gene, BNIP3, was analysed in terms of expression, effect on patient survival, and chemo-responsiveness in pancreatic cancer cell lines. cDNA microarray, real-time light cycler quantitative polymerase chain reaction, laser-capture microdissection, and immunohistochemistry analyses were used to evaluate BNIP3 expression in normal and diseased pancreatic specimens.
  • The effect of chemotherapeutic agents on pancreatic cancer cells was assessed utilizing 3-(4,5-methylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromide assays.
  • BNIP3 mRNA levels were 3.0- and 6.3-fold lower in chronic pancreatitis and pancreatic cancer compared to the normal pancreas, respectively.
  • Microdissection analysis confirmed the reduction of BNIP3 expression in pancreatic cancer cells compared to normal duct cells.
  • By immunohistochemistry, BNIP3 was predominantly expressed in the acinar cells of the normal and diseased pancreas.
  • Interestingly, while BNIP3 was undetectable in the cancer cells of 59% of the cases, 75-100% of PanIN2/3 lesions displayed BNIP3 immunoreactivity.
  • Hypoxia induced BNIP3 expression in four out of eight pancreatic cancer cell lines, while it was absent under normoxic and hypoxic conditions in the remaining four.
  • In conclusion, loss of BNIP3 expression occurs late in pancreatic cancer, contributes to resistance to chemotherapy, and correlates with a worsened prognosis.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Membrane Proteins / deficiency. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / deficiency. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Fluorouracil / pharmacology. Humans. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Survival Rate

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  • (PMID = 15856026.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNIP3 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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80. Shimizu K, Onishi M, Sugata E, Fujii H, Honoki K, Tsujiuchi T: Aberrant DNA methylation of the 5' upstream region of Tslc1 gene in hamster pancreatic tumors. Biochem Biophys Res Commun; 2007 Feb 9;353(2):522-6
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  • [Title] Aberrant DNA methylation of the 5' upstream region of Tslc1 gene in hamster pancreatic tumors.
  • To determine if the Tslc1 gene is involved in pancreatic carcinogenesis, the expression level of Tslc1 and the DNA methylation status of its 5' upstream region were investigated in pancreatic duct adenocarcinomas (PDAs) induced in hamsters by N-nitrosobis(2-oxopropyl)amine (BOP).
  • The expression level of Tslc1 was significantly reduced in PDAs (p < 0.05) compared with normal pancreatic tissues.
  • Although this region was unmethylated in normal pancreatic tissue, it was highly methylated in four PDAs, correlating with reduced Tslc1 expression.
  • [MeSH-major] 5' Untranslated Regions / genetics. DNA Methylation. DNA, Neoplasm / genetics. Immunoglobulins / genetics. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Cell Adhesion Molecules. Cricetinae. Female. Mesocricetus

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  • (PMID = 17187758.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / DNA, Neoplasm; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / Tumor Suppressor Proteins
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81. Ji Y, Kuang TT, Tan YS, Chen Y, Zeng HY, Jin DY: Pancreatic primary lymphoma: a case report and review of the literature. Hepatobiliary Pancreat Dis Int; 2005 Nov;4(4):622-6
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  • [Title] Pancreatic primary lymphoma: a case report and review of the literature.
  • BACKGROUND: Primary pancreatic lymphoma is a rare but treatable malignancy (less than 1% of pancreatic tumors) that may be clinically confused with pancreatic adenocarcinoma.
  • METHODS: In a patient with upper abdominal pain, ultrasonography and CT detected a mass in pancreatic head, which compressed the common bile duct.
  • RESULTS: Grossly the tumor involved the pancreatic head, soft in consistence and invaded part of the gastric wall.
  • Histologically, the tumor was composed mainly of large and moderate neoplastic cells, which were diffusely positive for CD20 and Bcl-6 antigens, indicating the features of diffusely large B cell lymphoma.
  • [MeSH-major] Lymphoma / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 16286277.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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82. Pitman MB, Michaels PJ, Deshpande V, Brugge WR, Bounds BC: Cytological and cyst fluid analysis of small (&lt; or =3 cm) branch duct intraductal papillary mucinous neoplasms adds value to patient management decisions. Pancreatology; 2008;8(3):277-84
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  • [Title] Cytological and cyst fluid analysis of small (< or =3 cm) branch duct intraductal papillary mucinous neoplasms adds value to patient management decisions.
  • BACKGROUND/AIM: Management of patients with small (1-3 cm) branch duct intraductal papillary mucinous neoplasms (IPMN) is a challenge.
  • Symptoms, dilated duct, mural nodule or positive cytology have been proposed as parameters for resection.
  • None were associated with a dilated duct and none had positive cytology.
  • CONCLUSIONS: The presence of a mural nodule in a small branch duct IPMN is a predictor of malignancy and invasion by univariate analysis.
  • Recognition of an atypical epithelial cell component in contrast to positive cytology or a cyst fluid CEA of >2,500 ng/ml is more accurate than the recommended algorithm and adds value to the preoperative assessment of clinically diagnosed small branch duct IPMN. and IAP.
  • [MeSH-major] Adenocarcinoma, Mucinous / chemistry. Adenocarcinoma, Mucinous / pathology. Pancreatic Cyst / pathology. Pancreatic Ducts / chemistry. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / pathology

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18497541.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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83. Sato M, Okumura T, Kaito K, Kiyoshima M, Asato Y, Uchiumi K, Iijima H, Hashimoto I, Kaburagi T, Amemiya R: Usefulness of FDG-PET/CT in the detection of pancreatic metastases from lung cancer. Ann Nucl Med; 2009 Jan;23(1):49-57
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  • [Title] Usefulness of FDG-PET/CT in the detection of pancreatic metastases from lung cancer.
  • OBJECTIVE: The objective of this study was to assess the ability to detect pancreatic metastasis of lung cancer and to clarify the degree of fluorodeoxyglucose (FDG) accumulation and computed tomography (CT) characteristics of pancreatic metastasis from lung cancer.
  • METHODS: A total of 573 patients (415 men and 158 women) with lung cancer were retrospectively evaluated.
  • RESULTS: Abnormal accumulations in the pancreas were detected in 5 of 313 patients (1.60%) in the initial study group, and 6 of 260 patients (2.31%) in the follow-up study group.
  • Seven of these patients had adenocarcinoma, three had small cell carcinoma, and the rest had large cell endocrine carcinoma.
  • Three of these pancreatic lesions were difficult to determine by routine transaxial images, and detection was obvious only by thin-slice images or multiplanar reconstruction images.
  • In addition, 10 of 11 cases did not show main pancreatic duct dilatation even if the tumor size was large.
  • CONCLUSIONS: Metastases to the pancreas in lung cancer patients are not so rare and radiologists first have an important role to detect the pancreatic mass and then suggest to metastasis as the likely diagnosis.
  • For this purpose, FDG-PET/CT has an advantage in depicting unsuspected pancreatic metastasis from lung cancer, particularly that which is not detected by CT alone.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / secondary. Fluorodeoxyglucose F18. Lung Neoplasms / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / secondary. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 19205838.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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84. Willmore-Payne C, Volmar KE, Huening MA, Holden JA, Layfield LJ: Molecular diagnostic testing as an adjunct to morphologic evaluation of pancreatic ductal system brushings: potential augmentation for diagnostic sensitivity. Diagn Cytopathol; 2007 Apr;35(4):218-24
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  • [Title] Molecular diagnostic testing as an adjunct to morphologic evaluation of pancreatic ductal system brushings: potential augmentation for diagnostic sensitivity.
  • Malignancies arising from the pancreatic and biliary ductal systems present the gastroenterologist and pathologist with diagnostic challenges.
  • Tumors of the pancreatic and/or biliary ductal system may present as either duct strictures or mass lesions.
  • Using the high resolution melting curve technique, we performed mutational analysis on 20 bile duct brushing specimens for mutations in p53, K-ras, BRAF, and EGFR genes.
  • Our series included twelve adenocarcinomas, one islet cell tumor, one case of dysplasia, and six benign cases.
  • No EGFR or B-raf mutations were detected and only a single p53 mutation in an adenocarcinoma was detected in the corresponding cytology specimen.
  • Mutational analysis did not appear to improve the cytologic detection of adenocarcinoma by bile duct brushings.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Pancreatic Ductal / genetics. Molecular Diagnostic Techniques. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / genetics


85. Pimenova EL, Bogatyrev VN, Chistiakova OV: [Evaluation of the diagnostic significance of cytologic studies in pancreatic tumors]. Klin Lab Diagn; 2006 Apr;(4):32-6
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  • [Title] [Evaluation of the diagnostic significance of cytologic studies in pancreatic tumors].
  • The study was undertaken to specify cytomorphological criteria for prostatic duct adenocarcinoma (PDAC), by assessing fine-needle aspiration biopsy (FNAB) specimens.
  • For statistical analysis, the authors selected the following cytological signs of malignancy: anisonucleosis, increased nuclei, hyperchromia, uneven chromatin distribution, enucleation, uneven nuclear outline, apocytes; increased nucleoli, nucleolar polymorphism, multiple nucleoli, increased cells, anisocytosis (polymorphism of the size and shape of a cell, mitoses, piled nuclei, papillary structures, slightly glandular structures.
  • [MeSH-major] Adenocarcinoma / diagnosis. Pancreatic Ducts / pathology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 16756163.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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86. Daniel SV, Vani DH, Smith AM, Hill QA, Menon KV: Obstructive jaundice due to a pancreatic mass: a rare presentation of acute lymphoblastic leukaemia in an adult. JOP; 2010;11(1):72-4
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  • [Title] Obstructive jaundice due to a pancreatic mass: a rare presentation of acute lymphoblastic leukaemia in an adult.
  • Liver function tests showed an obstructive picture, full blood count was normal and on computerised tomography there was diffuse enlargement of the pancreas, with dilatation of the common bile duct and intra hepatic biliary radicles.
  • Four weeks after presenting, the white cell count became elevated with blasts on the blood film and bone marrow biopsy revealed a precursor B cell acute lymphoblastic leukaemia.
  • After induction chemotherapy his jaundice resolved, the pancreatic mass reduced in size and he is now in a complete remission.
  • CONCLUSION: Acute lymphoblastic leukaemia may mimic common causes of a pancreatic mass such as adenocarcinoma and should be considered as part of the differential diagnosis when atypical features are present.
  • [MeSH-major] Jaundice, Obstructive / diagnosis. Pancreatic Diseases / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male. Organ Size. Pancreas / pathology

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  • (PMID = 20065559.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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87. Sawey ET, Johnson JA, Crawford HC: Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway. Proc Natl Acad Sci U S A; 2007 Dec 4;104(49):19327-32
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  • [Title] Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.
  • Acinar-to-ductal metaplasia in the pancreas is associated with an increased risk for tumorigenesis.
  • Molecular dissection of this process in vitro has shown that primary acinar cells, in response to EGF receptor ligands, can transdifferentiate into duct-like epithelia, passing through a nestin-positive intermediate, in a Notch pathway-dependent manner.
  • MMP-7 was found to be required for Notch activation, which leads to dedifferentiation of acinar cells to the nestin-positive transitional cell.
  • Besides being necessary for acinar transdifferentiation, it was found that MMP-7 activity was sufficient to induce the process, indicating that molecular signals capable of initiating MMP-7 expression also have the potential to induce formation of metaplastic epithelia in the pancreas.